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        <title>Experimental Biology and Medicine | Physiology, Pathophysiology and Mechanisms of Disease section | New and Recent Articles</title>
        <link>https://www.ebm-journal.org/journals/experimental-biology-and-medicine/sections/physiology-pathophysiology-and-mechanisms-of-disease</link>
        <description>RSS Feed for Physiology, Pathophysiology and Mechanisms of Disease 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>2026-04-05T15:31:39.510+00:00</pubDate>
        <ttl>60</ttl>
        <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.2026.10788</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.2026.10755</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.2026.10847</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.2026.10810</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2026.10810</link>
        <title><![CDATA[Maternal diet-induced hypercholanemia alters gut microbiota and metabolome in adult female Western diet-fed offspring]]></title>
        <pubdate>2026-01-30T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Caroline Ovadia</author><author>Saraid McIlvride</author><author>Josca M. Schoonejans</author><author>Konstantina Spagou</author><author>Maria Gómez-Romero</author><author>Ann Smith</author><author>Georgia Papacleovoulou</author><author>Vanya Nikolova</author><author>Peter H. Dixon</author><author>Elaine Holmes</author><author>Julian R. Marchesi</author><author>Catherine Williamson</author>
        <description><![CDATA[Children of mothers with intrahepatic cholestasis of pregnancy (ICP) are more likely to develop metabolic disease later in life. Using a mouse model of gestational cholestasis, we previously found that 18-week-old offspring had metabolic alterations that were exacerbated in female offspring when challenged with a Western diet (WD). Microbiota changes are emerging as a potential mechanism for developmental programming, and the maternal gut microbiota is known to be altered in pregnancy and in ICP. We hypothesized that, in our model, the offspring gut microbiota is altered by maternal gestational disease, potentially impacting future offspring metabolic health. Female mice were fed a cholic acid (CA)-supplemented diet for 1 week preceding and throughout pregnancy to mimic gestational hypercholanemia. Female offspring were challenged with a WD from 12 to 18 weeks of age and cecal contents were collected for metataxonomics and metabolomic profiling. Maternal CA dietary supplementation was associated with markedly increased cecal sulfated bile acid species (up to 387-fold increase). Whilst WD-feeding of offspring was associated with a greater proportion of primary to secondary bile acids, and more tauro-conjugated bile acids than for offspring fed a normal diet, this adaptation to WD-feeding was not evident for those whose mothers were fed a CA-supplemented diet. Indeed, WD-fed offspring of CA-supplemented mothers had a >2-fold reduction in CA and dehydrocholic acid levels compared to those from NC-fed mothers. This corresponded with an altered profile of cecal microbiota, with clear separation of microbiotal profiles according to maternal diet in the WD-fed, but not NC-fed, offspring. This observational mouse study has shown that exposure to maternal hypercholanemia can significantly impact the effects of an obesogenic diet on offspring intestinal bile acid metabolism and gut microbiota, likely increasing their vulnerability to metabolic dysfunction when exposed to the “second hit” of an unhealthy postnatal environment.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2025.10489</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2025.10489</link>
        <title><![CDATA[Variational autoencoder enhanced analysis of energy metabolism and autophagy in exercising cardiomyocytes]]></title>
        <pubdate>2025-09-22T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Liquan Chen</author><author>Yun Yang</author>
        <description><![CDATA[Autophagy of myocardial cells involves the interaction of multiple molecular signaling pathways, and regulatory factors, while existing methods are difficult to handle. This study utilized the variational autoencoder (VAE) model to reveal the characteristic distribution of myocardial cell energy autophagy under different exercise conditions. First, this paper is based on mass spectrometry analysis, enzyme-linked immunosorbent assay ELISA (Enzyme-Linked Immunosorbent Assay) to determine the cardiomyocyte metabolite concentration data, and RNA-Seq (Ribonucleic Acid-Sequencing) to collect genes related to cardiomyocyte energy metabolism and autophagy expression data; in the VAE model, this paper utilizes the full connectivity layer to encode the data into potential representations, and reconstructs the numerical data through the numerical data decoder. The loss function is defined as the data reconstruction error and KL (Kullback-Leibler) scatter, and Adam is used to optimize the training process; the features are analyzed and the classification performance is verified under different motion conditions based on RF (Random Forest); the relationship between the features and metabolite concentration and gene expression is analyzed by LASSO (Least Absolute Shrinkage and Selection Operator) regression model to analyze the relationship between features and metabolite concentration and gene expression; the features in the latent space are downscaled using t-SNE (t-distributed Stochastic Neighbor Embedding) to visualize the feature distribution; finally, CRISPR-Cas9 (Clustered Regularly Interspaced Short Palindromic Repeats-Cas9) knockdown experiments to reveal the importance of AMPK, PGC1A, CPT1B, and SIRT1 in cardiomyocyte autophagy and energy metabolism, which provide potential targets for future gene-based therapies.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2025.10461</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2025.10461</link>
        <title><![CDATA[An approach to evaluate the effect of inflammatory microvesicles on Ca2+ handling in human-induced pluripotent stem cell-derived cardiomyocytes]]></title>
        <pubdate>2025-08-28T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Dania Fischer</author><author>Mishkaat Sha’sha’a</author><author>Judith Schenz</author><author>Aycan Tayan</author><author>Christina Mertens</author><author>Sebastian O. Decker</author><author>Nadia Gallenstein</author><author>Maximilian Dietrich</author><author>Trim Lajqi</author><author>Anna Hafner</author><author>Markus A. Weigand</author><author>Nina D. Ullrich</author>
        <description><![CDATA[Microvesicles (MV) isolated from septic individuals were observed to impact systemic hemodynamics and cardiac function. The aim of this in vitro study was to analyze the effects of TNFα-induced endothelial MV (TMV) and MV from septic patients (SMV) on beating frequency and Ca2+ transient kinetics of human-induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CM). MV were isolated from supernatants of TNFα-stimulated primary human pulmonary microvascular endothelial cells (HPMEC) and plasma from 20 sepsis patients by ultracentrifugation and quantified using flow cytometry. Spontaneous Ca2+ transients were measured in hiPSC-CM using the Ca2+-sensitive ratiometric indicator fura-2 at different time points of incubation with different MV concentrations. At 16 h of incubation, higher MV concentrations showed significant differences, especially regarding decay and beating frequency. Despite high variability, at 10 × 106 MV/mL and 16 h of incubation, TMV significantly decreased frequency compared to control MV (CMV). SMV from septic patients did not reveal any significant effects on Ca2+ transients under these experimental settings. MV isolated from control or TNFα-treated HPMEC affected Ca2+ handling and spontaneous activity of hiPSC-CM, however, the measured effects were not consistent throughout the different conditions. Further refinement of the experiment conditions is needed to specify the exact conditions for crosstalk between endothelium-derived MV and cardiomyocytes.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2025.10524</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2025.10524</link>
        <title><![CDATA[Natural killer cell subpopulations in the peripheral blood of single ventricle/hypoplastic left heart syndrome patients via single-cell RNA sequencing]]></title>
        <pubdate>2025-08-14T00:00:00Z</pubdate>
        <category>Brief Communication</category>
        <author>Hui-Qi Qu</author><author>Kushagra Goel</author><author>Kayleigh Ostberg</author><author>Diana J. Slater</author><author>Fengxiang Wang</author><author>James Snyder</author><author>Cuiping Hou</author><author>Garnet Eister</author><author>John J. Connolly</author><author>Michael March</author><author>Joseph T. Glessner</author><author>Charlly Kao</author><author>Hakon Hakonarson</author>
        <description><![CDATA[Natural Killer (NK) cells are integral components of the innate immune system, recognizing and eliminating virus-infected cells. They may play a crucial role in the immune response and contribute to the complications associated with Single Ventricle/Hypoplastic Left Heart Syndrome (SV/HLHS). Utilizing single-cell RNA sequencing (scRNA-seq), NK cells from peripheral blood mononuclear cells (PBMCs) were analyzed in three de-identified SV/HLHS cases and three healthy controls. This study identified two novel NK cell subpopulations that could not be detected by conventional scRNA-seq pipelines or traditional flow cytometry. These subpopulations exhibit distinct gene expression profiles linked to the heterogeneity of immune responsiveness and stress adaptation in NK cells. In SV/HLHS patients, one cluster showed a significant upregulation of androgen response and downregulation of heme metabolism compared to healthy controls. Our study offers new insights into the fine-tuning of immune modulation that could help mitigate complications in SV/HLHS. It suggests that while NK cells in SV/HLHS adapt to support survival in a challenging physiological environment, these adaptations may compromise their ability to effectively respond to additional stresses, such as infections and inflammation.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2025.10448</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2025.10448</link>
        <title><![CDATA[N-acetyl-L-cysteine improves mitochondrial and oxidative defects in the acadian variant of fanconi syndrome]]></title>
        <pubdate>2025-05-23T00:00:00Z</pubdate>
        <category>Brief Communication</category>
        <author>Inas Al-Younis</author><author>Rebeca Martín-Jiménez</author><author>Mehtab Khan</author><author>Yann Baussan</author><author>Caroline Jose</author><author>Yves Thibeault</author><author>Etienne Hebert-Chatelain</author>
        <description><![CDATA[The Acadian variant of Fanconi Syndrome (AVFS) is a rare genetic disorder characterized by renal deficiencies. AVFS is caused by a mutation to NDUFAF6 encoding a complex I assembly factor, and leading to metabolic alterations. We confirmed that fibroblasts derived from AVFS patients have lower complex I activity, mitochondrial membrane potential and cellular respiration. These mitochondrial defects were accompanied by higher levels of 8-hydroxy-2′deoxyguanosine, malondialdehyde and carbonyl, which are markers of oxidative damage to DNA, lipids and proteins, respectively. Thus, we hypothesized that the antioxidant N-Acetyl-L-cysteine (NAC) would reduce oxidative stress and mitochondrial defects in AVFS fibroblasts. Treatment with NAC during 5 days partially restored complex I activity, mitochondrial membrane potential and cellular respiration in AVFS fibroblasts. NAC also prevented oxidative damage in AVFS fibroblasts. This work shows for the first time that the physiopathology of AVFS includes high oxidative stress. It also reveals that NAC and other antioxidant-based strategies might represent an effective pharmacological treatment for AVFS.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2025.10490</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2025.10490</link>
        <title><![CDATA[Primary cilia and inflammatory response: unveiling new mechanisms in osteoarthritis progression]]></title>
        <pubdate>2025-04-28T00:00:00Z</pubdate>
        <category>Mini Review</category>
        <author>Yuyan Sun</author><author>Ziyu Luo</author><author>Yuanyuan Fu</author><author>ThaiNamanh Ngo</author><author>Wen Wang</author><author>Yuanrong Wang</author><author>Ying Kong</author>
        <description><![CDATA[Osteoarthritis (OA) is a common degenerative joint disease that can lead to chronic pain and disability. The pathogenesis of OA involves chronic low-grade inflammation, characterized by the degradation of chondrocytes, inflammation of the synovium, and systemic low-grade inflammation. This inflammatory response accelerates the progression of OA and contributes to pain and functional impairment. Primary cilia play a crucial role in cellular signal transduction and the maintenance of cartilage matrix homeostasis, and their dysfunction is closely linked to inflammatory responses. Given these roles, primary cilia may significantly contribute to the pathogenesis of OA. This review explores inflammation-associated signaling pathways in OA, including NF-κB, MAPK, JAK/STAT, and PI3K/AKT/mTOR signaling. In addition, we place particular emphasis on cilia-mediated inflammatory modulation in OA. Primary cilia mediate chondrocyte responses to mechanical loading and inflammatory cytokines via pathways including NF-κB, MAPK, TRPV4, and Hedgehog signaling. Notably, alterations in the length and incidence of primary cilia in chondrocytes during OA further underscore their potential role in disease pathogenesis. The identification of biomarkers and therapeutic targets related to primary cilia and inflammatory pathways offers new potential for the treatment and management of OA.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2025.10605</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2025.10605</link>
        <title><![CDATA[Retraction: Hydrogen-rich saline protects myocardium against ischemia/reperfusion injury in rats]]></title>
        <pubdate>2025-04-10T00:00:00Z</pubdate>
        <category>Retraction</category>
        <author>EBM Editorial Office </author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2025.10204</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2025.10204</link>
        <title><![CDATA[A study on the differences in the gut microbiota and metabolism between male and female mice in different stress periods]]></title>
        <pubdate>2025-02-11T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Yajun Qiao</author><author>Juan Guo</author><author>Qi Xiao</author><author>Jianv Wang</author><author>Xingfang Zhang</author><author>Xinxin Liang</author><author>Lixin Wei</author><author>Hongtao Bi</author><author>Tingting Gao</author>
        <description><![CDATA[The sex difference in depression has long been an unsolved issue. Women are twice as likely to suffer from depression as men. However, there were significant differences in the composition of gut microbiota between women and men. There is a lack of studies linking sex differences in depression to microbiota, and the specific mechanisms of this process have not been explained in detail. The main purpose of this study was to explore the gender differences in the intestinal tract of male and female depressed mice. In this study, chronic restraint stress (CRS) mouse models were used to simulate chronic stress, and behavioral tests were conducted, including the open field test (OFT), tail suspension test (TST) and forced swimming test (FST). Microbial diversity analysis and metabolomics were performed on collected mouse feces. The results showed that female mice were highly active and prone to anxious behavior before stress, and the levels of f-Rikenellaceae, f-Ruminococcaceae and 16α-hydroxyestrone were significantly different from those in male mice. After 21 days (Days) of stress, female mice showed depression-like behavior, and the levels of f-Erysipelotrichaceae, 5α-pregnane-3,20-dione, and 2-hydroxyestradiol were significantly different from those in male mice. After 14 days of stress withdrawal, the depression-like behavior continued to worsen in female mice, and the levels of 5α-pregnane-3,20-dione, estrone glucuronide and f-Erysipelotrichaceae were significantly different from those in male mice. In summary, female mice have stronger stress sensitivity and weaker resilience than male mice, which may be related to differences in bacterial diversity and estrogen metabolism disorders.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2024.10121</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2024.10121</link>
        <title><![CDATA[Legumain in cardiovascular diseases]]></title>
        <pubdate>2024-07-22T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Lei Zhou</author><author>Jianqiang Wu</author><author>Zairong Wei</author><author>Yuehong Zheng</author>
        <description><![CDATA[Cardiovascular diseases (CVDs) are the leading cause of death worldwide, having become a global public health problem, so the pathophysiological mechanisms and therapeutic strategies of CVDs need further study. Legumain is a powerful enzyme that is widely distributed in mammals and plays an important role in a variety of biological processes. Recent research suggests that legumain is associated with the occurrence and progression of CVDs. In this review, we provide a comprehensive overview of legumain in the pathogenesis of CVDs. The role of legumain in CVDs, such as carotid atherosclerosis, pulmonary hypertension, coronary artery disease, peripheral arterial disease, aortic aneurysms and dissection, is discussed. The potential applications of legumain as a biomarker of these diseases are also explored. By understanding the role of legumain in the pathogenesis of CVDs, we aim to support new therapeutic strategies to prevent or treat these diseases.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2024.10104</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2024.10104</link>
        <title><![CDATA[Vaporization of perfluorocarbon attenuates sea-water-drowning-induced acute lung injury by deactivating the NLRP3 inflammasomes in canines]]></title>
        <pubdate>2024-04-19T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Cheng-Cheng Su</author><author>Zhao-Rui Zhang</author><author>Jin-Xia Liu</author><author>Ji-Guang Meng</author><author>Xiu-Qing Ma</author><author>Zhen-Fei Mo</author><author>Jia-Bo Ren</author><author>Zhi-Xin Liang</author><author>Zhen Yang</author><author>Chun-Sun Li</author><author>Liang-An Chen</author>
        <description><![CDATA[Seawater-drowning-induced acute lung injury (SD-ALI) is a life-threatening disorder characterized by increased alveolar–capillary permeability, an excessive inflammatory response, and refractory hypoxemia. Perfluorocarbons (PFCs) are biocompatible compounds that are chemically and biologically inert and lack toxicity as oxygen carriers, which could reduce lung injury in vitro and in vivo. The aim of our study was to explore whether the vaporization of PFCs could reduce the severity of SD-ALI in canines and investigate the underlying mechanisms. Eighteen beagle dogs were randomly divided into three groups: the seawater drowning (SW), perfluorocarbon (PFC), and control groups. The dogs in the SW group were intratracheally administered seawater to establish the animal model. The dogs in the PFC group were treated with vaporized PFCs. Probe-based confocal laser endomicroscopy (pCLE) was performed at 3 h. The blood gas, volume air index (VAI), pathological changes, and wet-to-dry (W/D) lung tissue ratios were assessed. The expression of heme oxygenase-1 (HO-1), nuclear respiratory factor-1 (NRF1), and NOD-like receptor family pyrin domain containing-3 (NLRP3) inflammasomes was determined by means of quantitative real-time polymerase chain reaction (qRT-PCR) and immunological histological chemistry. The SW group showed higher lung injury scores and W/D ratios, and lower VAI compared to the control group, and treatment with PFCs could reverse the change of lung injury score, W/D ratio and VAI. PFCs deactivated NLRP3 inflammasomes and reduced the release of caspase-1, interleukin-1β (IL-1β), and interleukin-18 (IL-18) by enhancing the expression of HO-1 and NRF1. Our results suggest that the vaporization of PFCs could attenuate SD-ALI by deactivating NLRP3 inflammasomes via the HO-1/NRF1 pathway.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.ebm-journal.org/articles/10.3389/ebm.2024.10112</guid>
        <link>https://www.ebm-journal.org/articles/10.3389/ebm.2024.10112</link>
        <title><![CDATA[Calcium-sensing receptor-mediated macrophage polarization improves myocardial remodeling in spontaneously hypertensive rats]]></title>
        <pubdate>2024-04-05T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Jiaqi Zhao</author><author>Ning Lu</author><author>Yuanyuan Qu</author><author>Wei Liu</author><author>Hua Zhong</author><author>Na Tang</author><author>Jiayi Li</author><author>Lamei Wang</author><author>Dongmei Xi</author><author>Fang He</author>
        <description><![CDATA[Chronic inflammation is a key element in the progression of essential hypertension (EH). Calcium plays a key role in inflammation, so its receptor, the calcium-sensing receptor (CaSR), is an essential mediator of the inflammatory process. Compelling evidence suggests that CaSR mediates inflammation in tissues and immune cells, where it mediates their activity and chemotaxis. Macrophages (Mφs) play a major role in the inflammatory response process. This study provided convincing evidence that R568, a positive regulator of CaSR, was effective in lowering blood pressure in spontaneously hypertensive rats (SHRs), improving cardiac function by alleviating cardiac hypertrophy and fibrosis. R568 can increase the content of CaSR and M2 macrophages (M2Mφs, exert an anti-inflammatory effect) in myocardial tissue, reduce M1 macrophages (M1Mφs), which have a pro-inflammatory effect in this process. In contrast, NPS2143, a negative state regulator of CaSR, exerted the opposite effect in all of the above experiments. Following this study, R568 increased CaSR content in SHR myocardial tissue, lowered blood pressure, promoted macrophages to M2Mφs and improved myocardial fibrosis, but interestingly, both M1Mφs and M2Mφs were increased in the peritoneal cavity of SHRs, the number of M2Mφs remained lower than M1Mφs. In vitro, R568 increased CaSR content in RAW264.7 cells (a macrophage cell line), regulating intracellular Ca2+ ([Ca2+]i) inhibited NOD-like receptor family protein 3 (NLRP3) inflammasome activation and ultimately prevented its conversion to M1Mφs. The results showed that a decrease in CaSR in hypertensive rats causes further development of hypertension and cardiac damage. EH myocardial remodeling can be improved by CaSR overexpression by suppressing NLRP3 inflammasome activation and macrophage polarization toward M1Mφs and increasing M2Mφs.]]></description>
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