<?xml version="1.0" encoding="utf-8"?>
    <rss version="2.0">
      <channel xmlns:content="http://purl.org/rss/1.0/modules/content/">
        <title>Experimental Biology and Medicine | Translational Research section | New and Recent Articles</title>
        <link>https://www.ebm-journal.org/journals/experimental-biology-and-medicine/sections/translational-research</link>
        <description>RSS Feed for Translational Research section in the Experimental Biology and Medicine journal | New and Recent Articles</description>
        <language>en-us</language>
        <generator>Frontiers Feed Generator,version:1</generator>
        <pubDate>2026-04-19T00:06:32.912+00:00</pubDate>
        <ttl>60</ttl>
        <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.2025.10784</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2025.10784</link>
        <title><![CDATA[Beginning of a new era of synthetic messenger RNA therapeutics: Comprehensive insights on mRNA drug design, development and applications]]></title>
        <pubdate>2025-12-12T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Saumya Nishanga Heendeniya</author><author>Suxiang Chen</author><author>Saadia Bhatti</author><author>Qurat Ul Ain Zahra</author><author>Kamal Rahimizadeh</author><author>Bal Hari Poudel</author><author>Stephen D. Wilton</author><author>Rakesh N. Veedu</author>
        <description><![CDATA[Messenger RNA (mRNA) therapeutics have significantly transformed contemporary medicine, particularly through their role as the active component in the SARS-CoV-2 vaccine. This remarkable achievement is the culmination of extensive research conducted over many years by scientists. The widespread administration of the COVID-19 vaccine has further accelerated research into the precise therapeutic potential of mRNA technologies. Since mRNA doesn’t integrate with the host genome, the safety and versatility of mRNA-based therapeutics make them an iconic candidate in targeted therapies. Due to a surge in innovation efforts, biomodification of the molecular signatures of mRNAs like the 5′cap, untranslated regions (UTRs), and the poly(A) tail are being developed to increase translation efficacy. Recent advancements in chemical modifications, codon optimization techniques, and targeted delivery methods have significantly enhanced the stability of synthetic mRNAs while concurrently reducing their immunogenicity. Various mRNA manufacturing and synthesizing methods are investigated in this review, focusing on their scalability and limitations. mRNA therapeutic strategies can be divided into protein replacement, immune modulation, and cellular modulation. This review explores mRNA’s molecular landscape and comprehensive utility, including applications in both clinical trials and commercial sectors.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2025.10782</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2025.10782</link>
        <title><![CDATA[Therapeutic effects of mesenchymal stromal cell secretome in liver fibrosis with acute lung injury]]></title>
        <pubdate>2025-09-30T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Ane Caroline Ribeiro Novaes Martins</author><author>Karina Ribeiro Silva</author><author>Anna Carolina de Souza Pereira</author><author>Gustavo Claudino Paris</author><author>Ana Lúcia Rosa Nascimento</author><author>Verônica Aiceles</author><author>Erika Afonso Costa Cortez</author><author>Alessandra Alves Thole</author><author>Simone Nunes de Carvalho</author>
        <description><![CDATA[Chronic liver disease (CLD) is a widespread condition and liver fibrosis is a common hallmark. The COVID-19 pandemic has drawn awareness over emerging pathogens that pose severe risks for chronic disease patients, whose management is complicated because most drugs can overload liver metabolism, therefore therapeutic alternatives are needed. Aims: based on the difficulty of treating CLD patients during respiratory infections, this study focused on the therapeutic evaluation of adipose-derived mesenchymal stromal cell (ASC) secretome. Methods: the effects of ASC secretome were evaluated in a preclinical murine model of liver fibrosis induced by thioacetamide (TAA) and acute lung injury induced by lipopolysaccharide, using histological and cytokine profile analyses. ASC secretome exhibited therapeutic effects alleviating fibrogenesis and inflammation, decreasing plasmatic inflammatory markers (cytokines IL-6, IL-17A and TNF-α), and restoring immune homeostasis. The secretome reduced liver collagen accumulation and IL-6 levels and restored lung cytoarchitecture, decreasing levels of CD68 and TNF-α. These results provide a preclinical basis for potential clinical use of the ASC secretome and its products, advancing the concept of cell-free, systemically active interventions for complex tissue injuries, and reinforcing the potential of its paracrine factors to modify pathological responses and promote tissue regeneration in combined chronic-acute diseases.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2025.10735</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2025.10735</link>
        <title><![CDATA[Corrigendum: A double-edged effect of hypoxia on astrocyte-derived exosome releases]]></title>
        <pubdate>2025-07-23T00:00:00Z</pubdate>
        <category>Correction</category>
        <author>Yang Jie Tseng</author><author>Hui-Ju Huang</author><author>Chien-Hui Lin</author><author>Anya Maan-Yuh Lin</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2025.10559</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2025.10559</link>
        <title><![CDATA[A double-edged effect of hypoxia on astrocyte-derived exosome releases]]></title>
        <pubdate>2025-05-21T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Yang Jie Tseng</author><author>Hui-Ju Huang</author><author>Chien-Hui Lin</author><author>Anya Maan-Yuh Lin</author>
        <description><![CDATA[Exosomes are the smallest extracellular vesicles secreted from cells, carrying different cargos, including nucleic acids, proteins and others which transfer from cells to cells. The properties of exosomes depend on the donor cells. Hypoxia, referring to a sublethal and insufficient oxygen supply, reportedly influences exosome secretion of hypoxic cells. In the present study, we focused on the effects of hypoxia on exosomes obtained from CTX-TNA2 astrocyte cells exposed to different durations of hypoxia followed by normoxia as a model of hypoxic preconditioning. To evaluate the functions of exosomes, primary cultured cortical neurons were treated with hemin, a potent neurotoxin. Our sulforhodamine B assay showed that incubation of hemin (30 μM) consistently induced neuronal death. Co-incubation of exosomes from CTX-TNA2 cells subjected to 2 hr-hypoxia plus 6 hr-renormoxia (2H/6R exosomes), but not 12 hr-hypoxia plus 24 hr-renormoxia (12H/24R exosomes), attenuated hemin-induced cell death and reduction in growth associated protein 43 level (a biomarker of neurite outgrowth). Western blot assay demonstrated that 2H/6R exosomes attenuated hemin-induced elevations in inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) levels (two proinflammatory biomarkers) as well as heme oxygenase-1 (HO-1). In contrast, 12H/24R exosomes did not alter hemin-induced elevation in HO-1 but further augmented hemin-induced increases in iNOS and COX-2. Moreover, 2H/6R exosomes attenuated hemin-induced reduction in glutathione hydroperoxidase 4 (a biomarker of ferroptosis) and elevation in active caspase 3 (a biomarker of apoptosis) while 12H/24R exosomes did not effectively alter hemin-induced programed cell death. In conclusion, our study showed that 2H/6R exosomes possessed neuroprotective activities while 12H/24R exosomes had mild pro-inflammatory activities, suggesting that different hypoxic preconditionings influenced CTX-TNA2 cells which then secreted exosomes with differential biological activities. These findings highlight a double-edged role of hypoxia on exosome functions.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2025.10422</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2025.10422</link>
        <title><![CDATA[Gender difference in pre-clinical liver-directed gene therapy with lentiviral vectors]]></title>
        <pubdate>2025-04-25T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Efrain Guzman</author><author>Cheen Khoo</author><author>Deirdre O’Connor</author><author>Gayathri Devarajan</author><author>Sharifah Iqball</author><author>Bernard Souberbielle</author><author>Kyriacos Mitrophanous</author><author>Yatish Lad</author>
        <description><![CDATA[Viral vector-based therapies are effective therapeutics for the correction of several disorders, both in mouse models and in humans. Several pre-clinical studies have demonstrated differences in transduction efficiencies and therapeutic effect between male and female mice dosed with AAV-based gene therapy product candidates. Here, we report gender-specific transduction and transgene expression differences in mice dosed systemically with lentiviral vectors (LVV). Male mice systemically dosed with LVV carrying the reporter gene luciferase showed at least a 12-fold higher expression of luciferase and a higher vector copy number (VCN) in their livers compared with female mice. Lastly, PAHEnu2 male mice dosed with a LVV carrying the human phenylalanine hydroxylase (PAH) transgene were observed to have a higher VCN than their female littermates. These findings suggest that sex-based differences initially observed in AAV-mediated therapies also apply to LVV, but the exact mechanism remains to be determined.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2025.10254</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2025.10254</link>
        <title><![CDATA[The effects of major abdominal surgery on skeletal muscle mitochondrial respiration in relation to systemic redox status and cardiopulmonary fitness]]></title>
        <pubdate>2025-02-21T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Jia L. Stevens</author><author>Helen T. McKenna</author><author>Magdalena Minnion</author><author>Andrew J. Murray</author><author>Martin Feelisch</author><author>Daniel S. Martin</author>
        <description><![CDATA[More complex surgeries are being performed in increasingly sicker patients, resulting in a greater burden of postoperative morbidity. Delineating the metabolic and bioenergetic changes that occur in response to surgical stress may further our understanding about how humans respond to injury and aid the identification of resilient and frail phenotypes. Skeletal muscle biopsies were taken from patients undergoing hepato-pancreatico-biliary surgery at the beginning and end of the procedure to measure mitochondrial respiration and thiol status. Blood samples were taken at the same timepoints to measure markers of inflammation and systemic redox state. A sub-group of patients underwent cardiopulmonary exercise testing prior to surgery, and were assigned to two groups according to their oxygen consumption at anaerobic threshold (≤10 and >10 mL/kg/min) to determine whether redox phenotype was related to cardiorespiratory fitness. No change in mitochondrial oxidative phosphorylation capacity was detected. However, a 26.7% increase in LEAK (uncoupled) respiration was seen after surgery (P = 0.03). Free skeletal muscle cysteine also increased 27.0% (P = 0.003), while S-glutathionylation and other sulfur and nitrogen-based metabolite concentrations remained unchanged. The increase in LEAK was 200% greater in fit patients (P = 0.004). Baseline plasma inflammatory markers, including TNF-⍺ and IL-6 were greater in unfit patients, 96.6% (P = 0.04) and 111.0% (P = 0.02) respectively, with a 58.7% lower skeletal muscle nitrite compared to fit patients. These data suggest that oxidative phosphorylation is preserved during the acute intraoperative period. Increase in free cysteine may demonstrate the muscle’s response to surgical stress to maintain redox balance. The differences in tissue metabolism between fitness groups suggests underlying metabolic phenotypes of frail and resilient patients. For example, increased LEAK in fitter patients may indicate mitochondrial adaptation to stress. Higher baseline measurements of inflammation and lower tissue nitrite in unfit patients, may reflect a state of frailty and susceptibility to postoperative demise.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2025.10390</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2025.10390</link>
        <title><![CDATA[Is platelet-rich plasma better than steroids as epidural drug of choice in lumbar disc disease with radiculopathy? Meta-analysis of randomized controlled trials]]></title>
        <pubdate>2025-02-04T00:00:00Z</pubdate>
        <category>Mini Review</category>
        <author>Sathish Muthu</author><author>Vibhu Krishnan Viswanathan</author><author>Prakash Gangadaran</author>
        <description><![CDATA[The current meta-analysis was performed to analyze the efficacy and safety of platelet-rich plasma (PRP) as an epidural injectate, in comparison with steroids in the management of radiculopathy due to lumbar disc disease (LDD). We conducted independent and duplicate searches of the electronic databases (PubMed, Embase and Cochrane Library) in March 2024 to identify randomized controlled trials (RCTs) analyzing the efficacy of epidural PRP for pain relief in the management of LDD. Animal or in vitro studies, clinical studies without a comparator group, and retrospective or non-randomised clinical studies were excluded. Diverse post-intervention pain scores [visual analog score (VAS)] and functional scores [Oswestry Disability Index (ODI), SF-36], as reported in the reviewed studies, were evaluated. Statistical analysis was performed using STATA 17 software. 5 RCTs including 310 patients (PRP/Steroids = 153/157) were included in the analysis. The included studies compared the efficacy and safety of epidural PRP and steroids at various time-points including 1, 3, 6, 12, 24, and 48 weeks. Epidural PRP injection was found to offer comparable pain relief (VAS; WMD = −0.09, 95% CI [−0.66, 0.47], p = 0.641; I2 = 96.72%, p < 0.001), functional improvement (ODI; WMD = 0.72, 95% CI [-6.81, 8.25], p = 0.524; I2 = 98.73%, p < 0.001), and overall health improvement (SF-36; WMD = 1.01, 95% CI [−1.14, 3.17], p = 0.224; I2 = 0.0%, p = 0.36) as epidural steroid injection (ESI) at all the observed time points in the included studies without any increase in adverse events or complications. Epidural administration of PRP offers comparable benefit as epidural steroid injection (ESI) in the management of radiculopathy due to LDD. The safety profile of the epidural PRP is also similar to ESI.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2024.10361</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2024.10361</link>
        <title><![CDATA[Neuroinflammation underlies the development of social stress induced cognitive deficit in male sickle cell mice]]></title>
        <pubdate>2024-11-19T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>S’Dravious A. DeVeaux</author><author>Sofiya Vyshnya</author><author>Katherine Propsom</author><author>Oluwabukola T. Gbotosho</author><author>Asem S. Singh</author><author>Robert Z. Horning</author><author>Mihika Sharma</author><author>Anil G. Jegga</author><author>Liang Niu</author><author>Edward A. Botchwey</author><author>Hyacinth I. Hyacinth</author>
        <description><![CDATA[Cognitive deficit is a debilitating complication of sickle cell disease (SCD), with a multifactorial etiopathogenesis. Here we show that neuroinflammation and dysregulation in lipidomics and transcriptomics profiles are major underlying mechanisms of social stress-induced cognitive deficit in SCD. Male Townes sickle cell (SS) mice and controls (AA) were exposed to social stress using the repeat social defeat (RSD) paradigm concurrently with or without treatment with minocycline. Mice were tested for cognitive deficit using novel object recognition and fear conditioning tests. SS mice exposed to RSD without treatment had worse performance on cognitive tests compared to SS mice exposed to RSD with treatment or to AA controls, irrespective of their RSD or treatment disposition. Additionally, compared to SS mice exposed to RSD with treatment, SS mice exposed to RSD without treatment had significantly more cellular evidence of neuroinflammation coupled with a significant shift in the differentiation of neural progenitor cells towards astrogliogenesis. Additionally, brain tissue from SS mice exposed to RSD was significantly enriched for genes associated with blood-brain barrier dysfunction, neuron excitotoxicity, inflammation, and significant dysregulation in sphingolipids important to neuronal cell processes. We demonstrate in this study that social stress induces cognitive deficit in SS mice, concurrently with neuroinflammation and lipid dysregulation.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2024.10246</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2024.10246</link>
        <title><![CDATA[STEMIN and YAP5SA, the future of heart repair?]]></title>
        <pubdate>2024-10-31T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Nada Bejar</author><author>Siyu Xiao</author><author>Dinakar Iyer</author><author>Azeez Muili</author><author>Adeniyi Adeleye</author><author>Bradley K. McConnell</author><author>Robert J. Schwartz</author>
        <description><![CDATA[This review outlines some of the many approaches taken over a decade or more to repair damaged hearts. We showcase the recent breakthroughs in organ regeneration elicited by reprogramming factors OCT3/4, SOX2, KLF4, and C-MYC (OKSM). Transient OKSM transgene expression rejuvenated senescent organs in mice. OKSM transgenes also caused murine heart cell regeneration. A triplet alanine mutation of the N-terminus of Serum Response Factor’s MADS box SRF153(A3), termed STEMIN, and the YAP mutant, YAP5SA synergized and activated OKSM and NANOG in adult rat cardiac myocytes; thus, causing rapid nuclear proliferation and blocked myocyte differentiation. In addition, ATAC seq showed induced expression of growth factor genes FGFs, BMPs, Notchs, IGFs, JAK, STATs and non-canonical Wnts. Injected STEMIN and YAP5SA synthetic modifying mRNA (mmRNA) into infarcted adult mouse hearts, brought damaged hearts back to near normal contractility without severe fibrosis. Thus, STEMIN and YAP5SA mmRNA may exert additional regenerative potential than OKSM alone for treating heart diseases.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2024.10266</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2024.10266</link>
        <title><![CDATA[Bridging the gap: a translational perspective in spinal cord injury]]></title>
        <pubdate>2024-09-26T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Omar Imad Hassan</author><author>Soichiro Takamiya</author><author>Azam Asgarihafshejani</author><author>Michael G. Fehlings</author>
        <description><![CDATA[Traumatic spinal cord injury (SCI) is a devastating and complex condition to treat with no curative options. In the past few decades, rapid advancements in our understanding of SCI pathophysiology as well as the mergence of new treatments has created more optimism. Focusing on clinical translation, this paper provides a comprehensive overview of SCI through its epidemiology, pathophysiology, currently employed management strategies, and emerging therapeutic approaches. Additionally, it emphasizes the importance of addressing the heavy quality of life (QoL) challenges faced by SCI patients and their desires, providing a basis to tailor patient-centric forms of care. Furthermore, this paper discusses the frequently encountered barriers in translation from preclinical models to clinical settings. It also seeks to summarize significant completed and ongoing SCI clinical trials focused on neuroprotective and neuroregenerative strategies. While developing a cohesive regenerative treatment strategy remains challenging, even modest improvements in sensory and motor function can offer meaningful benefits and motivation for patients coping with this highly debilitating condition.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2024.10142</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2024.10142</link>
        <title><![CDATA[Potential therapeutic effects of peroxisome proliferator-activated receptors on corneal diseases]]></title>
        <pubdate>2024-06-27T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Bing Jie Chow</author><author>Isabelle Xin Yu Lee</author><author>Chang Liu</author><author>Yu-Chi Liu</author>
        <description><![CDATA[The cornea is an avascular tissue in the eye that has multiple functions in the eye to maintain clear vision which can significantly impair one’s vision when subjected to damage. Peroxisome proliferator-activated receptors (PPARs), a family of nuclear receptor proteins comprising three different peroxisome proliferator-activated receptor (PPAR) isoforms, namely, PPAR alpha (α), PPAR gamma (γ), and PPAR delta (δ), have emerged as potential therapeutic targets for treating corneal diseases. In this review, we summarised the current literature on the therapeutic effects of PPAR agents on corneal diseases. We discussed the role of PPARs in the modulation of corneal wound healing, suppression of corneal inflammation, neovascularisation, fibrosis, stimulation of corneal nerve regeneration, and amelioration of dry eye by inhibiting oxidative stress within the cornea. We also discussed the underlying mechanisms of these therapeutic effects. Future clinical trials are warranted to further attest to the clinical therapeutic efficacy.]]></description>
      </item>
      </channel>
    </rss>