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        <title>Experimental Biology and Medicine | New and Recent Articles</title>
        <link>https://www.ebm-journal.org/journals/experimental-biology-and-medicine</link>
        <description>RSS Feed for Experimental Biology and Medicine | New and Recent Articles</description>
        <language>en-us</language>
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        <pubDate>2026-04-17T02:16:08.165+00:00</pubDate>
        <ttl>60</ttl>
        <item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.11021</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.11021</link>
        <title><![CDATA[CAR T cell engineering approaches to minimise toxicities]]></title>
        <pubdate>2026-04-15T00:00:00Z</pubdate>
        <category>Mini Review</category>
        <author>Elizabeth Hogben</author><author>Anna Schurich</author><author>Charlotte Graham</author>
        <description><![CDATA[For the treatment of many forms of cancer, cell- and gene-based therapies are showing promise in both pre-clinical data and clinical trials. In particular, CAR T cell therapies, of which there are now 7 FDA-approved products, have shown ground-breaking results in haematological cancers such as multiple myeloma and B cell malignancies. Recent research is also attempting to develop effective CAR T cell therapies for solid tumours, with varying success. One of the key challenges faced by CAR T cell therapy is balancing strong cytotoxic activity for an effective treatment with preventing severe and potentially lethal toxicities, such as Cytokine Release Syndrome and Immune Effector Cell-Associated Neurotoxicity Syndrome. This mini review discusses some of the potential solutions that scientists have devised to overcome toxicities and improve existing CAR T cell therapies.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.10850</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.10850</link>
        <title><![CDATA[Lymphatic pumping technique in mice alters blood parameters and metastatic melanoma in an age-dependent manner]]></title>
        <pubdate>2026-03-30T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Christopher Walsh</author><author>Matthew Kirstein</author><author>Elise Wagner</author><author>Emily Scott</author><author>Jerome Walsh</author><author>Shashank Reddy</author><author>Nathan Hoggard</author><author>Arshad Ahmad</author><author>Reetobrata Basu</author><author>Sam Mathes</author><author>Yanrong Qian</author><author>John J. Kopchick</author>
        <description><![CDATA[Therapeutic touch applied to primary tumors can increase metastasis. The goal of this project was to determine whether touch applied to metastatic tumors also increases metastasis. We evaluated touch on a mouse model of experimental metastasis using a manual treatment called Lymphatic Pumping Technique (LPT), which increases lymphatic fluid flow and is contraindicated in patients with cancer. The LPT, or a sham treatment, was administered for 5 minutes while the mice were anesthetized with vaporized isoflurane. Young adult (3 months old) and aged (20–24 months old) mice received daily sham or LPT treatments for 7 days prior to the injection of 200k B16F10-luc2 mouse melanoma cells into the tail vein, then treated every other day for 21 days. In middle-aged (9–11 months old) mice, we waited 8 days after tumor injection to start treatments and assessed the effect of LPT on immunotherapy efficacy. These mice also received either LPT or sham every other day, along with four doses of 200 µg anti–PD-1 or isotype control antibody. LPT did not increase tumor growth or spread in any of the experiments. Surprisingly, LPT was negatively associated with metastasis in young and middle-aged mice, without enhancing or diminishing the efficacy of immunotherapy. In mice without cancer, LPT rapidly elevated red blood cell, white blood cell, and platelet counts in young, but not middle-aged, animals. Taken together, these findings suggest that therapeutic touch near metastatic tumors does not worsen disease and may confer an age-dependent benefit.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.10857</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.10857</link>
        <title><![CDATA[Towards a standardized diabetic prolonged wound healing model in hairless SKH1 mice]]></title>
        <pubdate>2026-03-20T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Elle Koivunotko</author><author>Julia Monola</author><author>Chris S. Pridgeon</author><author>Jere Linden</author><author>Riina Harjumäki</author><author>Emrah Yatkin</author><author>Mari Madetoja</author><author>Marjo Yliperttula</author>
        <description><![CDATA[Chronic wounds, particularly those associated with diabetes, pose a significant clinical challenge due to their impaired healing dynamics and lack of reliable and standardized preclinical models. This pilot study aimed to establish a diabetogenic, immunocompetent, hairless mouse model (SKH1 strain) to simulate prolonged wound healing. Diabetes was induced by streptozotocin administration, followed by the creation of full-thickness dorsal skin wounds. Wounds were treated with either saline or nanofibrillated cellulose hydrogel as a model treatment. Wound healing progression and blood glucose were monitored, and histopathological assessments were performed after a 14-day experiment. In addition, for the first time, the Thermidas thermal imaging system was used in an in vivo mouse model to evaluate skin temperature. Results demonstrated that diabetes induction successfully prolonged wound closure by 5 days compared with the previously described acute wound model in the same strain with the identical protocol without streptozotocin (STZ) induction. Histopathological analyses showed increased macrophage activity (16.2% vs. 2.2% in the treatment groups and 10.2% vs. 0.3% in the control groups) and decreased collagen deposition (12.2% vs. 43.2% in the treatment groups and 17.6% vs. 27.4% in the control groups), suggesting prolonged wound healing. These findings support the use of hairless SKH1 mice as a viable model for studying prolonged diabetic wound healing and evaluating future therapeutic candidates.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.10933</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.10933</link>
        <title><![CDATA[Genetics of epilepsy]]></title>
        <pubdate>2026-03-19T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Kynen Piacentini</author><author>Athanasios Gaitatzis</author><author>Sulev Kõks</author>
        <description><![CDATA[Epilepsy is one of the most common neurological diseases in the world, but it is also complex and difficult to study. There is a significant genetic component to epilepsy and more information is being published frequently. It is difficult to group and summarise all of this information in a way that is beneficial for both researchers and clinicians. The aim of this paper is to create a summary of all currently known epilepsy associated genes in order to aid epilepsy research to better understand the aetiology of the disease. This was achieved through gathering genetic data from three databases: Online Mendelian Inheritance in Man (OMIM), Clincal Genome (ClinGen), and PubMed. Genes were filtered based on specific criteria and were summarised into three tables: Epilepsy genes, Epilepsy associated genes and Predicted epilepsy associated genes. A fourth table was produced to showcase all epilepsy genes that were identified in all three databases. A total of 2,536 genes were identified to have some level of association with epilepsy. A total of 238 genes were classified as Epilepsy genes, 1,317 genes were classified as Epilepsy associated genes and 981 genes were classified as Predicted epilepsy genes. Finally, 86 genes were identified to be epilepsy genes that were found in all three genetic databases and represent the highest confidence in association with epilepsy. The significance of this study involves the ability to give researchers an up-to-date list of genes that have an association to epilepsy and a summary of information about said genes.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.10907</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.10907</link>
        <title><![CDATA[A novel platelet-rich plasma clinically induces reliable, rapid, long-term chronic peripheral neuropathic pain elimination]]></title>
        <pubdate>2026-03-13T00:00:00Z</pubdate>
        <category>Brief Communication</category>
        <author>Damien P. Kuffler</author><author>Onix Reyes</author><author>Ivan J. Sosa</author><author>Christian A. Foy</author>
        <description><![CDATA[Peripheral nerve trauma results in 50%–84% of patients developing chronic neuropathic pain, which is eliminated when axons reinnervate targets. Autografts reduce pain by promoting target reinnervation. We hypothesized that applying a novel platelet-rich plasma (PRP) formulation to proximal stumps would permanently eliminate the pain. This prospective case series compared analgesia levels after bridging nerve gaps with an autograft (autograft repair) vs. a PRP-filled collagen tube (PRP repair). Autograft repairs were performed on 16 nerves with a 5.75-cm mean gap length, 2.0-year repair delay, 42.3-year age, and 8.6 chronic neuropathic pain. PRP repairs were performed on 10 nerves with a 6.0-cm gap length, 1-year repair delay, 36.7-year age, with 88% having 9.1 chronic neuropathic pain. For autograft repairs, the pain began to decrease when axons reinnervated targets, reaching a mean of 0.3 in 18.2% of patients, and was eliminated in 81.8%. Following PRP repairs, the pain reduction began within 2 weeks and was eliminated by 2 months. Thus, autografts contribute to pain reduction/elimination by promoting target reinnervation. However, PRP directly and rapidly induced long-term pain elimination in all patients, while axons were regenerating, and without target reinnervation. These results prove that platelet-released factors reliably and rapidly eliminate chronic neuropathic pain.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.10796</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.10796</link>
        <title><![CDATA[Enhanced oxidative stress resilience in C. elegans acox-1.1 mutants through CTL-3 and proteasomal regulation]]></title>
        <pubdate>2026-03-13T00:00:00Z</pubdate>
        <category>Brief Communication</category>
        <author>Woori Bae</author><author>Mina Norman</author><author>Myon Hee Lee</author>
        <description><![CDATA[Oxidative stress is a primary driver of aging, necessitating robust cellular adaptation mechanisms. While peroxisomal β-oxidation and proteasomal degradation are known to influence stress responses, their functional crosstalk remains elusive. In this study, we show that C. elegans acox-1.1 mutants, despite having a shortened lifespan under normal conditions, exhibit a paradoxical resistance to mild chronic oxidative stress (1 mM paraquat, PQ) compared to wild-type worms. This PQ-induced resistance in acox-1.1 mutants was independent of the canonical SKN-1 pathway but required the peroxisomal catalase CTL-3. RNA-mediated knockdown of ctl-3 largely abolished the stress resistance of acox-1.1 mutants, leading to rapid mortality. Proteomic and biochemical analyses revealed that acox-1.1 mutants possess reduced levels of PAS-5, a core 20S proteasome subunit, resulting in impaired proteasomal assembly and accumulation of ubiquitinated (Ub) substrates under basal conditions. Intriguingly, exposure to 1 mM PQ significantly reduced the Ub-smear in acox-1.1 mutants, suggesting a metabolic shift where the cell prioritizes ROS scavenging over ATP-dependent protein degradation. Under oxidative stress, acox-1.1 mutants bypass defective proteasomal machinery and redirect energy toward CTL-3-mediated antioxidant defense. This study identified a peroxisomal adaptation mechanism whereby reduced proteasome complexity, coupled with enhanced ROS-regulatory machinery, confers survival advantages under specific oxidative challenges.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.10679</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.10679</link>
        <title><![CDATA[Low dose thirdhand smoke exposure enhances platelet functional responses in mice]]></title>
        <pubdate>2026-03-12T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Precious O. Badejo</author><author>Ahmed B. Alarabi</author><author>Hamdy E. A. Ali</author><author>Lanam Millican</author><author>Reina De La Paz</author><author>Shelby S. Umphres</author><author>Sadia Kamal</author><author>Fatima Z. Alshbool</author><author>Fadi T. Khasawneh</author>
        <description><![CDATA[Although cigarette smoking is the most preventable cause of cardiovascular diseases, most researchers have focused on either direct/firsthand or secondhand smoke exposures. Recently though, attention has shifted to an emerging/indirect exposure trend-known as thirdhand smoke (THS)- which was previously “overlooked.” This phenomenon, which was/is thought to be harmless, has been identified as a serious health risk, including in the context of thrombogenesis/platelets. However, whether low dose THS exposure has the capacity to modulate platelets has not been investigated. Two sets of household materials were exposed to 20 cigarettes/day for a week on an alternating basis, with controls exposed to clean air. After the first set of exposed materials is placed in mice cages, exposure of the second set is initiated. The materials were interchanged weekly, for a total exposure duration of 1 month. Mice were then subjected to multiple platelet function assays. THS exposed mice exhibited shortened tail bleeding and occlusion times, indicating a prothrombotic phenotype. Moreover, we also observed that platelets from the exposed mice exhibited an enhanced aggregation response. However, we did not observe any gender differences in our in vivo as well as aggregation experiments; hence, subsequent characterization was carried out on male mice. It was also found that dense granules release, integrin activation, and PS exposure were also potentiated in the exposed platelets compared to the controls. Finally, we observed for the first time that the tobacco-specific nitrosamine and THS toxicant NNK enhanced platelet aggregation and thrombus formation. Collectively, we provide documentation that low dose of THS exposure is detrimental to health by increasing the risk of thrombosis through a hyperactive platelet phenotype that involves the toxicant NNK.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.10867</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.10867</link>
        <title><![CDATA[Metabolomics-guided identification of bioactive phytometabolites from South African plants targeting neuroblastoma]]></title>
        <pubdate>2026-03-05T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Mmei Cheryl Motshudi</author><author>Clarissa Marcelle Naidoo</author><author>Chikwelu Lawrence Obi</author><author>Benson Chucks Iweriebor</author><author>Earl Prinsloo</author><author>Muhammad Sulaiman Zubair</author><author>Nqobile Monate Mkolo</author>
        <description><![CDATA[Neuroblastoma constitutes a solid tumor in pediatric populations, characterized by a dismal prognosis and a scarcity of effective therapeutic interventions. Medicinal flora from South Africa represents valuable sources of bioactive phytometabolites with potential relevance to neuroblastoma. This study employed an integrated workflow merging untargeted UPLC-MS/MS metabolomics, mitochondrial functional assays, and in silico absorption, distribution, metabolism, and excretion (ADME) prediction to systematically identify bioactive metabolites from Acorus calamus and Lippia javanica with activity against SH-SY5Y neuroblastoma cells. Cytotoxic effects were quantified utilizing the CCK-8 assay, while mitochondrial membrane potential (ΔΨm) was conducted through JC-1 flow cytometry. Untargeted UPLC-MS/MS profiling yielded metabolomic fingerprints, through PCA, PLS-DA, and OPLS-DA. ADME and drug-likeness were predicted using SWISSADME. Both plant extracts exhibited dose-dependent inhibition of SH-SY5Y cell viability, with IC50 values determined at 0.2886 μg/μL for A. calamus and 0.3066 μg/μL for L. javanica. The ΔΨm assessment indicated enhanced mitochondrial polarization (68.2% and 65.4% compared to 58.8% in untreated controls), implying modulation of mitochondrial functional status. Metabolomic profiling unveiled distinct phytochemical signatures, including flavonoids, phenolics, jasmonates, and alkaloids, exhibiting significant species-level differentiation (F = 936.71, R2 = 0.989, p = 0.005). Notable metabolites such as isopropyl β-glucoside, 6β-hydroxymethandienone, and 7-epi-12-hydroxyjasmonic acid demonstrated favorable ADME characteristics and permeability across the blood-brain barrier. This investigation elucidates that A. calamus and L. javanica possess potential efficacy against neuroblastoma, underscoring the translational potential of African medicinal flora in pediatric oncology and necessitating further preclinical exploration.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.10929</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.10929</link>
        <title><![CDATA[Global MyoG research 2004–2024: a bibliometric analysis of trends and translational implications]]></title>
        <pubdate>2026-03-05T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Luoming Hu</author><author>Weizhong Zhuang</author><author>Weimin Chen</author><author>Song Yang</author><author>Shuo Chen</author><author>Xin Wang</author><author>Qiang Gao</author><author>Jimei Chen</author>
        <description><![CDATA[Myogenin (MyoG) is a core myogenic transcription factor that orchestrates myoblast differentiation and myofiber maturation and has been increasingly implicated in skeletal muscle degeneration and rhabdomyosarcoma, yet its global research landscape has not been systematically characterized. In this study, we performed a bibliometric analysis of MyoG-related publications from 2004 to 2024 retrieved from the Web of Science Core Collection. A total of 402 articles authored by 2,402 researchers from 1,148 institutions across 165 countries and regions were analyzed using VOSviewer, CiteSpace and R-based bibliometric tools. We quantified annual publication output, identified leading countries, institutions, authors and journals, and reconstructed collaboration, co-citation and keyword co-occurrence networks to delineate thematic evolution. The global pattern showed a multipolar structure dominated by the United States and China, with European institutions forming an additional hub and emerging countries contributing with growing but comparatively lower impact. Research hotspots exhibited a clear progression from early work on molecular mechanisms (DNA binding, MyoD family interactions, chromatin remodelling) toward regenerative biology (satellite cell regulation, muscle regeneration) and, more recently, disease-oriented studies focused on muscle atrophy, Duchenne muscular dystrophy and rhabdomyosarcoma. Landmark co-cited studies established MyoG as an indispensable regulator of skeletal muscle differentiation and highlighted its expanding relevance in pathological remodelling and therapeutic targeting. Future work is expected to concentrate on decoding MyoG-centred regulatory networks in degenerative muscle disease, integrating single-cell and spatial transcriptomics with functional genomics and multi-omics, and developing MyoG-based diagnostic and targeted therapeutic strategies. Despite the intrinsic limitations of single-database and citation-based approaches, this study provides a panoramic overview of two decades of MyoG research and offers a structured framework to guide future basic and translational investigations in muscle biology and oncology.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.10834</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.10834</link>
        <title><![CDATA[A novel de novo ATP2B1 variant causes autosomal dominant intellectual developmental disorder 66 by disrupting calcium homeostasis via impaired membrane trafficking]]></title>
        <pubdate>2026-03-03T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Huanhuan Zang</author><author>Xiaoyun Yang</author><author>Yucai Liu</author><author>Caiyun Ma</author><author>Dawei Yang</author>
        <description><![CDATA[Heterozygous pathogenic variants in ATP2B1 (encoding PMCA1) cause autosomal dominant intellectual developmental disorder 66 (MRD66; OMIM #619910). To date, only 12 pathogenic de novo ATP2B1 variants have been reported in MRD66. This study aimed to identify the genetic etiology in a Chinese infant with a neurodevelopmental disorder characterized by early-onset seizures and global developmental delay (GDD) and functionally characterize a novel ATP2B1 missense variant. Trio-based whole-exome sequencing revealed a heterozygous de novo ATP2B1 variant (c.2140A>C, p.Thr714Pro) in the proband. The proband presented with infantile spasms, GDD (Gesell Developmental Quotient: 65–74), and severe growth restriction (height/weight <−2 SD). To investigate the variant’s pathogenicity, the wild-type (WT) and mutant ATP2B1 constructs, N-terminally tagged with mScarlet, were transfected into HEK293T cells. Confocal imaging demonstrated profound cytoplasmic mislocalization of the p.Thr714Pro mutant protein, contrasting sharply with the characteristic plasma membrane localization of WT ATP2B1. Measurement of intracellular Ca2+ levels using Fluo-4 AM showed a significant 2.07-fold increase in basal Ca2+ levels in cells expressing the mutant compared to WT. This finding expands the spectrum of ATP2B1 variants associated with MRD66 and confirms calcium dyshomeostasis as the core pathomechanism. This case of MRD66 demonstrates a very early onset of seizures, consistent with the recognized phenotypic variability and the critical role of PMCA1 in early neurodevelopment.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.10701</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.10701</link>
        <title><![CDATA[Ananalysis of the effects of Treg cell therapy intervention on the gut microbiota of type 1 diabetic mice using 16S rRNA gene sequencing]]></title>
        <pubdate>2026-03-03T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Mengyao Zhou</author><author>Kang Du</author><author>Hanmin Wang</author><author>Zhuxian Zhang</author><author>Rui Zhao</author><author>Chenghong Ma</author><author>Qionger Huang</author><author>Wei Zhang</author><author>Weiwen Chen</author>
        <description><![CDATA[This study established a type 1 diabetes (T1DM) mouse model via intraperitoneal injection of streptozotocin (STZ) and examined the effect of regulatory T (Treg) cells on the gut microbiota by comparing its composition and diversity across three groups: control, T1DM, and Treg-treated mice. Forty-one 8-week-old male C57BL/6 mice under specific pathogen-free conditions were divided into a healthy control group, an untreated T1DM group, and a Treg treatment group (receiving low, medium, or high doses). T1DM was induced by administering a low-dose STZ injection over five consecutive days, with diabetes confirmation defined as a blood glucose level ≥300 mg/dL. CD4+CD25+ Treg cells isolated from spleens of healthy mice were used for treatment. Fecal samples collected on days 0, 14, and 34 from three randomly selected mice per group were subjected to 16S rRNA gene sequencing targeting the V3-V4 regions. The results showed significant differences in both alpha and beta diversity among the groups. Dominant bacterial families varied: Ruminococcaceae and others were enriched in the Treg treatment group, Muribaculaceae in the control group, and Lactobacillaceae in the untreated T1DM group. Genus-level abundances also shifted over time. Firmicutes abundance positively correlated with Treg levels (r = 0.70, p = 0.0433) but negatively with IFN-γ, whereas Cyanobacteria exhibited the opposite correlation. The Firmicutes/Bacteroidetes ratio was higher in T1DM mice than in controls and lower in the Treg-treated group. Metabolic pathway analysis indicated that two-component systems and ABC transporters were more prevalent in T1DM mice. In summary, Treg cell treatment altered the diversity, composition, dominant taxa, and Firmicutes/Bacteroidetes ratio of the gut microbiota compared with untreated T1DM mice.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.10709</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.10709</link>
        <title><![CDATA[Identification of potential hub genes related to ferroptosis and hypoxia in dilated cardiomyopathy: a bioinformatic analysis with preliminary experimental validation]]></title>
        <pubdate>2026-03-02T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Xiqin Wang</author><author>Chrismis Novalinda Ginting</author><author>William Leslie</author>
        <description><![CDATA[The study aims to explore the potential role of ferroptosis and hypoxia in dilated cardiomyopathy (DCM). GSE120895, GSE17800, GSE112556, ferroptosis-related genes (FRGs), and hypoxia-related genes (HRGs) were downloaded from the public dataset. Ferroptosis- and hypoxia-related differentially expressed genes (DEGs) and DCM-related genes were obtained. Subsequentially, hub genes were identified, and their diagnostic values were assessed. Next, immune cell infiltration analysis, drug prediction and molecular docking were carried out based on the hub genes. Finally, the hub gene TGM2 was preliminarily verified in vitro. A total of 18 ferroptosis- and hypoxia-related DEGs and 315 DCM-related genes were acquired. Subsequently, 6 hub genes (PPP1R15A, TGM2, MAP3K5, USP7, SESN2, and ADAM23) were obtained and have potential diagnostic value. Immune infiltration analysis showed that CD56dim natural killer (NK) cells, macrophages, monocytes, NK cells, and NK T cells were significantly infiltrated in DCM patients. Furthermore, the lncRNA-miRNA-mRNA network was constructed. Moreover, 16 drugs were predicted, and the binding energy between atorvastatin and TGM2 was −2.79 kcal/mol. In vitro verification showed that TGM2, PPP1R15A and SESN2 were up-regulated in DOX-induced AC16 cardiomyocyte injury. After knocking down TGM2, the expressions of α-actinin and cTnT were increased, and the expression level of HIF-1α was inhibited. Dual luciferase assay showed that hsa-miR-291-5p exerted its regulatory effect by directly binding to TGM2. Flow cytometry results showed that TGM2 had no significant effect on the apoptosis of AC16 cells. Our findings may provide new ideas for the diagnosis and treatment of DCM.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.10835</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.10835</link>
        <title><![CDATA[Skeletal muscle reprogramming in peripheral nerve injury: mechanisms, therapeutic roles, and complication management]]></title>
        <pubdate>2026-03-02T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Fuqiang Long</author><author>Xiaoru Pan</author><author>Anxin He</author><author>Xinlu Wang</author><author>Zairong Wei</author><author>Shaoying Gao</author>
        <description><![CDATA[Peripheral nerve injury (PNI) presents a significant clinical challenge, frequently leading to long-term neuromuscular dysfunction, muscle atrophy, fibrosis, and chronic pain. Traditional repair strategies, including microsurgical reconnection and neurotrophic support, often yield limited functional recovery, especially in cases of delayed or incomplete reinnervation. In this context, skeletal muscle reprogramming—defined as the intentional modulation of cellular fate, function, or metabolic state in muscle-resident cells—has emerged as a promising strategy to enhance regenerative outcomes. This process involves transcriptional, epigenetic, and metabolic interventions targeting myogenic progenitors, fibro-adipogenic progenitors (FAPs), satellite cells (MuSCs), and the broader muscle microenvironment. Recent studies demonstrate that reprogramming strategies can mitigate denervation-induced muscle atrophy, delay fibrotic remodeling, promote neuromuscular junction (NMJ) reconstruction, and even stimulate endogenous nerve regrowth via retrograde signaling. Mechanistic insights have uncovered pivotal roles for signaling pathways such as Wnt/β-catenin, TGF-β, Notch, and HDAC-regulated chromatin dynamics. Furthermore, innovations in small molecule cocktails, CRISPR-based transcriptional reactivation, and metabolic rewiring have expanded the therapeutic toolkit for muscle preservation and regeneration. This review comprehensively examines the molecular mechanisms, therapeutic roles, and translational challenges of skeletal muscle reprogramming in the context of PNI. We explore how muscle-targeted interventions can address complications of denervation, improve the efficacy of nerve repair, and offer a synergistic axis of regeneration when integrated with nerve-centric strategies. Finally, we identify key knowledge gaps and outline future research directions required to translate reprogramming-based therapies into clinical practice.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.10755</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.10755</link>
        <title><![CDATA[L-Glutamine attenuates peritoneal fibrosis developed in 5-Fluorouracil-treated mice]]></title>
        <pubdate>2026-02-24T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Juliana Francisca Grossi Heleno</author><author>Leticia Cristine Cardoso dos Santos</author><author>Igor Campos Fontes</author><author>Mirielly Ranny Almeida Paiva Silva</author><author>Lucas Barbosa Correia</author><author>Nayma Drielly Granato Silva</author><author>Pedro Henrique Dias Moura Prazeres</author><author>Pedro Pires Goulart Guimarães</author><author>Derek W. Gilroy</author><author>Silvia Passos Andrade</author><author>Paula Peixoto Campos</author>
        <description><![CDATA[Peritoneal fibrosis is an adverse effect of cancer therapy leading to progressive organ failure. L-Glutamine supplementation has been shown to attenuate fibrosis and improve wound healing in several types of tissue injuries. The aim of this study was to evaluate the effects of this supplementation on key components of the peritoneal fibrovascular tissue induced by implants in mice treated with 5-Fluorouracil (5-FU) C57BL/6 mice received three intraperitoneal doses of immunosuppressant (60, 40, and 40 mg/kg) on non-consecutive days prior to implantation of polyether-polyurethane sponges into the peritoneal cavity. The group treated with L-Glutamine received 150 mg/kg/day for 7 days (oral gavage) starting 24 h after implantation and the control group received filtered water. Eight days after implantation, implants were removed and processed for inflammatory, angiogenic, and fibrogenic markers. Flow cytometry results showed that L-Glutamine decreased (48%) the frequency/influx of total intra-implant cells. The remaining cell population in the treated group had more neutrophils, lymphocytes, and macrophages than in the control. Immunohistochemistry analysis showed fewer Caspase-3-positive cells in the treated group. Myeloperoxidase (MPO) and N-acetyl-β-D-glucosaminidase (NAG) activities, TNF-α levels, and mast cell numbers were decreased in the implants of the L-Glutamine-treated group compared with the control. Similarly, angiogenesis (VEGF levels and number of blood vessels) was attenuated by L-Glutamine. Supplementation also decreased the amount of intra-implant collagen and TGF-β1 levels. These results indicate that L-Glutamine attenuates critical inflammatory-angiogenesis and profibrotic pathways involved in fibrosis development in immunosuppression conditions, supporting its potential as an adjunct therapeutic strategy for managing peritoneal healing in cancer.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.10788</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.10788</link>
        <title><![CDATA[Intra- and extrapulmonary lipopolysaccharides-induced acute lung injury and pharmacotherapeutic response patterns in ventilated 7-day-old rabbits]]></title>
        <pubdate>2026-02-24T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Guiyin Zhuang</author><author>Qiang Gu</author><author>Siyu Xie</author><author>Xiaojing Guo</author><author>Bo Sun</author>
        <description><![CDATA[We explored pharmacotherapeutic response patterns of lipopolysaccharides (LPS)-induced pneumonia and sepsis as direct and indirect acute lung injury (ALI), and efficacy of a combined surfactant (S) and inhaled nitric oxide (iNO), simulating critical care, in rabbits of post-neonatal infancy. Anaesthetized 7-day-old healthy rabbits were injected intratracheally (IT) or intravenously (IV) with LPS (15–20–25 mg/kg, L) or saline as a control (C), and subjected to initial 2-hour mechanical ventilation (MV) with standardized tidal volume to induce ALI. They were then treated with S (200 mg/kg) and iNO (10 ppm, N), or not, thereby allocating to 6 groups (ITC, ITL, ITLSN, IVC, IVL, IVLSN) for another 8 h. Survival time/rate (ST), and variables as biomarkers in lung physiology, histopathology, biochemistry, and pathophysiology were measured. The survival was LPS-route, but not dosing, dependent. Compared to the IVL, ITL had relatively higher ST, lung injury score (LIS), lower intrapulmonary phospholipid pools, mRNA expressions in surfactant proteins (SPs) and pulmonary vascular endothelial cell injury (VEI)-related variables. ITLSN had higher phospholipid pools but no improvement in ST, lung mechanics, LIS or mRNA expression of SPs, proinflammatory mediators and VEI-related variables. IVLSN had improved lung mechanics, LIS, phospholipid pools, and SP-A mRNA expression, but worse ST, metabolic acidosis, higher interleukin mRNA expression in the lungs, liver and kidney, suspected as sepsis-associated multiorgan involvement. Using the infant rabbit LPS-ALI model, we characterized the survival as LPS-route dependent, the lung impairment and response pattern in surfactant and iNO treatment ineffectiveness/failure, as pharmacotherapeutic response patterns, with causal implication pertinent to the underlying pathophysiology of experimental pediatric ARDS.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.10894</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.10894</link>
        <title><![CDATA[The effect of short-term consumption of Bifidobacterium bifidum on the gut microbiome of obese individuals]]></title>
        <pubdate>2026-02-23T00:00:00Z</pubdate>
        <category>Brief Communication</category>
        <author>Inna Burakova</author><author>Yuliya Smirnova</author><author>Polina Morozova</author><author>Svetlana Pogorelova</author><author>Olga Kryukova</author><author>Tatiana Kislova</author><author>Olga Korneeva</author><author>Mikhail Syromyatnikov</author>
        <description><![CDATA[It is known that gut microbiota dysbiosis can lead to obesity by disrupting energy consumption and metabolism. Probiotic supplements are a potential therapeutic option for improving intestinal homeostasis. The aim of this study was to investigate the effect of a probiotic supplement containing Bifidobacterium bifidum on the intestinal microbiome of people with obesity using high-throughput sequencing on the DNBSEQ-G50 platform. The study demonstrated a positive effect of the supplement on bacterial species such as Bacteroides uniformis, Alistipes putredinis, Alistipes shahii, Dysosmobacter welbionis, and Gemmiger formicilis. Therefore, we suggest the potential use of this bacterial species in the treatment of gut microbiota dysbiosis of obese individuals.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.10847</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.10847</link>
        <title><![CDATA[The gut-retina axis in age-related macular degeneration: immune crosstalk and metabolite production]]></title>
        <pubdate>2026-02-23T00:00:00Z</pubdate>
        <category>Mini Review</category>
        <author>Beryl Zhou</author><author>Zaid Parekh</author><author>Christopher Phung</author><author>Sarah H. Rodriguez</author><author>Dimitra Skondra</author>
        <description><![CDATA[Current therapies slow down advanced features but do not halt or reverse degeneration and neovascularization in dry and wet age-related macular degeneration (AMD). Recent research implicates the gastrointestinal microbiome as a potential critical modulator in AMD pathogenesis through the gut-retina axis. Dysbiosis, characterized by imbalanced microbial diversity, composition and function, can exacerbate systemic and retinal inflammation through microglial priming, inflammasome activation, and secretion of pro-angiogenic cytokines (IL-6, IL-1β, TNF-α, VEGF). Additionally, microbiome-derived metabolites such as short-chain fatty acids and bile acids may exert modulatory roles in host immunity and homeostasis. Their depletion in conjunction with enrichment of specific microbial taxa have been linked to progression of advanced AMD. Together, these complex systems of immune crosstalk in relation to dysbiosis highlight the gut-retina axis as a promising therapeutic target. Dietary modifications, particularly Mediterranean and high-fiber diets, enhance production of protective metabolites and are associated with decreased AMD progression risk compared to Western dietary patterns. Experimental strategies such as fecal microbiota transplantation in animal models and drug repurposing strategies show promise in modulating disease severity. This review synthesizes current mechanistic insights into microbial-immune crosstalk in AMD, emphasizing the interplay of dysbiosis, immune activation, and metabolite signaling.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.10745</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.10745</link>
        <title><![CDATA[Poliovirus receptor (PVR) expression as a predictor of relapse in colorectal cancer: bioinformatics and virtual screening]]></title>
        <pubdate>2026-02-13T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Sulaiman S. Alhudaithi</author><author>Muhamed Hamza R. Salih</author><author>Zaid H. AlHusseini</author><author>Sarah M. Almufadhili</author><author>Noura Alelayani</author><author>Ahmed H. Bakheit</author><author>Hamad M. Alkahtani</author><author>Hanadi H. Asiri</author><author>Ali A. Alshamrani</author><author>Ali R. Alhoshani</author><author>Moureq R. Alotaibi</author><author>Homood M. As Sobeai</author>
        <description><![CDATA[Colorectal cancer (CRC) is one of the most frequently diagnosed malignancies worldwide. Despite advancements in CRC treatment strategies in recent years, disease recurrence remains a major problem; relapsed patients have a poorer prognosis and higher mortality risk. Several factors have been associated with CRC relapse. However, the role of immune checkpoints in CRC recurrence remains elusive. In this work, we aimed to investigate immune checkpoint genes correlated with recurrence in CRC, evaluate their potential as prognostic biomarkers, and identify promising immune checkpoint inhibitors through molecular docking and molecular dynamics simulations. Clinical, genetic, and epigenetic data of relapsed and relapse-free CRC patients in the Cancer Genome Atlas were retrieved from the cBioportal database and evaluated. Subsequently, molecular docking and molecular dynamics simulations studies were conducted to identify suitable poliovirus receptor (PVR)/TIGIT binders. PVR is a ligand for TIGIT and competes with CD226. The crystal structure used for docking was obtained from the Protein Data Bank (PDB ID: 3UDW). Using this investigative approach, clinical parameters data revealed that among immune checkpoint genes, the PVR gene was significantly upregulated in relapsed patients. That upregulation was strongly correlated with diagnosis age, Aneuploidy, fraction genome alterations, and mutation count. Furthermore, free survival analysis showed that patients exhibiting elevated PVR levels were 2.16 times more likely to relapse than those with low PVR expression (p = 0.039). Virtual screening identified 106 natural compounds as potential binders at the PVR/TIGIT interface. Molecular docking and molecular dynamics simulations identified three binders that exhibit favorable interactions with PVR, with ZINC001848443492 emerging as the most promising. The results underscore the potential role of PVR as a prognostic biomarker for relapse in CRC. Future studies, including TIGIT-PVR blockade assays and assessments of the impact of predicted PVR/TIGIT interface binders on T cell function, are necessary to validate this study’s findings.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.10712</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.10712</link>
        <title><![CDATA[Electrotherapy in the management of neuropathic corneal pain: narrative review]]></title>
        <pubdate>2026-02-06T00:00:00Z</pubdate>
        <category>Review</category>
        <author>A. V. Shanmathi</author><author>Mingyi Yu</author><author>Chang Liu</author><author>Isabelle Xin Yu Lee</author><author>Louis Tong</author><author>Yu-Chi Liu</author>
        <description><![CDATA[Neuropathic corneal pain (NCP) is a debilitating condition resulting from corneal nerve damage or dysfunction, leading to persistent ocular pain, discomfort and hypersensitivity. Conventional therapy with eye drops often provides inadequate relief, necessitating the need for alternative therapeutic approaches. This review explores the role of electrotherapy in managing NCP, including its mechanisms, clinical efficacy, and potential integration into multimodal treatment strategies. We examine current evidence on various electrotherapy modalities such as transcutaneous electrical nerve stimulation, neurostimulation, and microcurrent stimulation. These electrotherapies have the potential to modulate pain pathways, promote nerve regeneration, and restore corneal homeostasis. Emerging studies suggest electrotherapy may alleviate NCP by altering neural signaling and reducing hyperalgesia. Integrating electrotherapy into existing pain management strategies may enhance the outcomes for patients with refractory NCP. However, its clinical application remains limited by a lack of standardized protocols and robust clinical trials. Although electrotherapy presents a promising and non-invasive option for NCP management, further research is needed to optimize the treatment parameters and optimal duration, assess the long-term efficacy, and establish guidelines for clinical use.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2026.10938</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.10938</link>
        <title><![CDATA[How can we balance risk and benefit of interleukin-18 armored T cell therapies?]]></title>
        <pubdate>2026-02-06T00:00:00Z</pubdate>
        <category>Mini Review</category>
        <author>Paulina Vicenova</author><author>John Maher</author>
        <description><![CDATA[CD19-specific CAR T cells engineered to secrete a constitutively active form of the pro-inflammatory cytokine, interleukin (IL)-18 have demonstrated impressive efficacy in a recent clinical trial involving subjects who had failed prior CAR T cell therapy. Corroborating these clinical data, preclinical studies of IL-18-armored CAR and T cell receptor-engineered T cells have demonstrated enhanced anti-tumor activity in several xenograft and syngeneic mouse cancer models. Interleukin-18 improves tumor clearance via direct effects on CAR T cells and indirect actions on cells on a variety of host immune cells, including natural killer, macrophage and dendritic cells. Compared to unarmored CAR T cells, IL-18-secreting CAR T cells are less exhausted, expand more efficiently and produce greater quantities of interferon (IFN)-γ. However, upregulated circulating IL-18 and its downstream mediator, IFN-γ, are also associated with systemic toxicities which have proven to be severe on occasions. In light of this, several groups have developed strategies that set out to restrict IL-18 release or biological activity to the tumor microenvironment. Among these, CAR T cells armored with NFAT-inducible IL-18 are now undergoing clinical testing. The evaluation of inducible or tumor-selective IL-18 deployment will show whether it is possible to minimize IL-18 related systemic toxicities while preserving localized amplification of anti-tumor activity.]]></description>
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