Cellular and Molecular Gastroenterology and Hepatology最新文献

{"title":"Reduced Intestinal GLP-1+ Cell Numbers Are Associated With an Inflammation-related Epithelial Metabolic Signature","authors":"Elisabeth Urbauer ,&nbsp;Doriane Aguanno ,&nbsp;Katharina Kuellmer ,&nbsp;Amira Metwaly ,&nbsp;Nadine Waldschmitt ,&nbsp;Mohamed Ahmed ,&nbsp;Sevana Khaloian ,&nbsp;Gabriele Hörmannsperger ,&nbsp;Julien Planchais ,&nbsp;Tobias Fromme ,&nbsp;R. Balfour Sartor ,&nbsp;Harry Sokol ,&nbsp;Dirk Haller ,&nbsp;Eva Rath","doi":"10.1016/j.jcmgh.2025.101656","DOIUrl":"10.1016/j.jcmgh.2025.101656","url":null,"abstract":"<div><h3>Background &amp; Aims</h3><div>Enteroendocrine cells (EECs) are known for their role in digestion and metabolism, yet their role in intestinal inflammation remains unclear. In inflammatory bowel diseases, a contribution of EECs to pathogenesis is indicated by autoantibodies affecting EEC function and general disease symptoms like insulin resistance and altered intestinal motility. Particularly, the L cell-derived hormone glucagon-like peptide 1 (GLP-1), suggested to orchestrate metabolic-inflammatory responses may influence inflammatory pathways in the intestine.</div></div><div><h3>Methods</h3><div>We quantified numbers of GLP-1⁺ cells in 4 different mouse models of intestinal inflammation and performed transcriptional analyses of colonic epithelial cells from inflamed interleukin-10-deficient mice. Using a publicly available single-cell RNA sequencing dataset including mucosal biopsies from patients with Crohn’s disease, we confirmed findings from the murine models. A model of mitochondrial dysfunction (ClpP^ΔIEC mice) as well as murine and human intestinal organoids were used to study molecular mechanisms.</div></div><div><h3>Results</h3><div>Numbers of GLP-1 expressing cells are consistently reduced at the site of active disease in mouse models and patients with Crohn’s disease. Despite this reduction, L cells from inflamed interleukin-10-deficient mice remained functional regarding GLP-1 secretion. Transcriptional analyses of intestinal epithelial cells indicate altered differentiation correlating with an inflammatory metabolic fingerprint. Reduced GLP-1⁺ cells in ClpP^ΔIEC mice and inhibition of respiration in organoid cultures supports a causative role for metabolism in steering differentiation.</div></div><div><h3>Conclusions</h3><div>Reduction of GLP-1⁺ cells represents a general feature of ileal and colonic inflammation in mice and humans. Given the numerous properties of GLP-1, this reduction likely affects inflammatory processes in the mucosa and disease-related symptoms on multiple levels, and therefore, should be considered a therapeutic target in inflammatory bowel diseases.</div></div>","PeriodicalId":55974,"journal":{"name":"Cellular and Molecular Gastroenterology and Hepatology","volume":"20 2","pages":"Article 101656"},"PeriodicalIF":7.1,"publicationDate":"2025-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145233609","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Human-length Telomeres Limit Regeneration of Liver Epithelial Cells in Mice","authors":"Michael Y. Hu ,&nbsp;Melissa Rowe ,&nbsp;Mark Tigue ,&nbsp;Yitzhak Reizel ,&nbsp;Riham Smoom ,&nbsp;Yehuda Tzfati ,&nbsp;Klaus H. Kaestner","doi":"10.1016/j.jcmgh.2025.101655","DOIUrl":"10.1016/j.jcmgh.2025.101655","url":null,"abstract":"<div><h3>Background &amp; Aims</h3><div>Telomeres, or the ends of linear chromosomes, are critical for maintaining genomic integrity. The commonly used C57BL/6 mouse strain has telomeres about 5 times longer than those present in humans. We recently engineered the C57BL/6 “Telomouse” to enable the study of human length telomeres, which we used here to study the effects of shortened telomeres on liver regeneration.</div></div><div><h3>Methods</h3><div>We performed partial hepatectomy experiments with Telomice using wild type C57BL/6 mice as controls. Staggered injections of the thymidine analogs 5-chloro-2'-deoxyuridine (CldU) and 5-iodo-2'-deoxyuridine (IdU) were used to analyze their incorporation into nuclear DNA during cells’ S-phase to assess proliferation. In a second model, we employed a competitive hepatocyte repopulation assay in fumarylacetoacetate hydrolase (Fah) null mice.</div></div><div><h3>Results</h3><div>We found that human-length telomeres limit the proliferative capacity of cholangiocytes and hepatocytes in short-term liver regeneration. Control mice exhibited significant cholangiocyte proliferation at 36 hours post-partial hepatectomy (PHx), which remained stable at 46 hours post-PHx. In contrast, Telomice exhibited decreased cholangiocyte proliferation at 36 hours post-PHx, which further decreased at 46 hours post-PHx. Both control and Telomice exhibit increased hepatocyte proliferation at 46 hours compared with 36 hours post-PHx. However, Telomice exhibit less proliferation than controls at both time points. Compared with controls, Telomice exhibit an increased DNA damage response in the liver after partial hepatectomy. In a second model, Telomice hepatocytes also exhibited reduced efficacy in a competitive repopulation study using the Fah null mouse model of conditional hepatocyte ablation.</div></div><div><h3>Conclusions</h3><div>Short telomeres induce DNA damage in the regenerating liver, hampering its ability to accelerate cell proliferation and regenerate the liver.</div></div>","PeriodicalId":55974,"journal":{"name":"Cellular and Molecular Gastroenterology and Hepatology","volume":"20 2","pages":"Article 101655"},"PeriodicalIF":7.1,"publicationDate":"2025-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145214081","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Activation and Spatial Redistribution of RNA Splicing Factors Trigger Hepatic Regeneration","authors":"Yachun An ,&nbsp;Jiabei Lian ,&nbsp;Wenjing Wei ,&nbsp;Yunuo Mao ,&nbsp;Longxin Qiao ,&nbsp;Tingting Li ,&nbsp;Ruijian Li ,&nbsp;Shumin Li ,&nbsp;Shigang Zhao ,&nbsp;Xuena Chen ,&nbsp;Han Zhao ,&nbsp;Huili Hu","doi":"10.1016/j.jcmgh.2025.101654","DOIUrl":"10.1016/j.jcmgh.2025.101654","url":null,"abstract":"<div><h3>Background &amp; Aims</h3><div>Tissue injury with regenerative obstacle leads to liver failure and inevitable consequent hepatic diseases. Yet, precise spatial and molecular alterations to initiate liver regeneration remain unknown.</div></div><div><h3>Methods</h3><div>We employed spatiotemporal sequencing of regenerating liver combined with high-throughput single-cell RNA sequencing of established hepatocyte organoids (Hep-Orgs) mimicking the regenerative start, elucidate that splicing factors (SFs) were key factors responsible for liver regeneration. Additionally, we verify the function of splicing factors in knockout mice models in vivo.</div></div><div><h3>Results</h3><div>We observed that the upregulation of SFs in regenerative zone of liver and precycling or cycling hepatocytes subpopulation of Hep-Orgs. We demonstrated that the splicing inhibitors suppress liver regeneration by increasing ribosomal proteins. Moreover, we identified HNRNPU as the key SF for liver regeneration benefit to preventing chronic liver diseases like metabolic dysfunction-associated steatotic liver disease.</div></div><div><h3>Conclusions</h3><div>The spatial remodeling of upregulated RNA SFs drives the first regenerative wave from the periportal zone. The reprogrammed subpopulations defined by highly expressed SFs represent original repopulating hepatocytes. Inhibiting RNA splicing leads to cellular upregulation of ribosomal proteins (RPs), less proliferative signals, and abnormal lipid accumulation. Knockout of SFs leads to failure of liver regeneration and zonal disorder. SF reduction marks severe metabolic dysfunction-associated steatotic liver disease in patients and knockout mouse models. Our results lay the molecular foundation for tissue repair initiation and further developing potential therapeutic targets for liver disease.</div></div>","PeriodicalId":55974,"journal":{"name":"Cellular and Molecular Gastroenterology and Hepatology","volume":"20 2","pages":"Article 101654"},"PeriodicalIF":7.1,"publicationDate":"2025-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145208176","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Long Noncoding RNA uc173 is a Novel Regulator of Mitochondrial Metabolism Driving Intestinal Mucosal Growth","authors":"Lan Xiao ,&nbsp;Song Ah Chae ,&nbsp;Dongyoon Yoo ,&nbsp;Hee K. Chung ,&nbsp;Min S. Kwon ,&nbsp;Amy VanderStoep ,&nbsp;Ting-Xi Yu ,&nbsp;Bridgette Warner ,&nbsp;Myriam Gorospe ,&nbsp;Jian-Ying Wang","doi":"10.1016/j.jcmgh.2025.101653","DOIUrl":"10.1016/j.jcmgh.2025.101653","url":null,"abstract":"<div><h3>Background &amp; Aims</h3><div>Long noncoding RNA <em>uc.173</em>, transcribed from ultraconserved regions, modulates many cell processes central to human pathologies, but the mechanism underlying <em>uc.173</em> in the homeostasis of the intestinal epithelium is underexplored. Here, we investigated the role of <em>uc.173</em> in regulating mitochondrial metabolism and defined the implication of altered mitochondrial activity by <em>uc.173</em> in renewal of the intestinal mucosa.</div></div><div><h3>Methods</h3><div>Studies were conducted in CRISPR-Cas9 knock-in mice, primary enterocytes, and Caco-2 cells. Mitochondrial structure and function were elucidated by measuring mitochondria-associated proteins and mitochondrial respiratory capacity. Intestinal mucosal growth was measured by Ki67 immunostaining or BrdU incorporation assays.</div></div><div><h3>Results</h3><div>Transient and specific deletion of <em>uc.173</em> in the intestinal epithelium of mice by CRISPR-Cas9 knock-in using small guide RNA decreased the levels of several mitochondria-associated proteins including PGC-1α, along with disrupted mucosal growth. Decreasing the levels of <em>uc.173</em> in cultured intestinal epithelial cells also decreased mitochondrial proteins and caused defects in the mitochondrial respiratory capacity. Reinforcing mitochondrial activity by using a mitochondrial activator or by overexpressing PGC-1α rescued growth of <em>uc.173</em>-deficient intestinal organoids. Mechanistic studies revealed that <em>uc.173</em> increased PGC-1α expression by acting as a molecular decoy for miR-29b, thereby preventing the repressive interaction of miR-29b with <em>PGC-1α</em> mRNA.</div></div><div><h3>Conclusions</h3><div>These findings indicate that <em>uc.173</em> is a novel regulator of mitochondrial metabolism in the intestinal epithelium and highlight a role of deregulation of <em>uc.173</em>, miR-29b, and PGC-1α in the suppressed renewal of intestinal mucosa in patients with critical illnesses.</div></div>","PeriodicalId":55974,"journal":{"name":"Cellular and Molecular Gastroenterology and Hepatology","volume":"20 2","pages":"Article 101653"},"PeriodicalIF":7.1,"publicationDate":"2025-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145208284","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"HIF-2α-driven Lipogenesis and Inflammation in Metabolic Dysfunction-associated Steatotic Liver Disease: Role of ATF4 Signaling","authors":"Zhe Yang ,&nbsp;Niujian Wu ,&nbsp;Xin Li ,&nbsp;Yun Li ,&nbsp;Zhanjin Lu ,&nbsp;Taoping Sun ,&nbsp;Zhixing Cao ,&nbsp;Xianghong Wang ,&nbsp;Chen Yang ,&nbsp;Shisong Han ,&nbsp;Hongyun Lu","doi":"10.1016/j.jcmgh.2025.101651","DOIUrl":"10.1016/j.jcmgh.2025.101651","url":null,"abstract":"<div><h3>Background &amp; Aims</h3><div>Metabolic dysfunction-associated steatotic liver disease (MASLD) is characterized by an imbalance of lipid metabolism and chronic inflammation. Emerging evidence suggests a role for hypoxia-inducible factor 2α (HIF-2α) in MASLD progression. However, the mechanistic linkage between HIF-2α and steatohepatitis progression remains largely elusive.</div></div><div><h3>Methods</h3><div>Here, hepatocyte-specific HIF-2α knockout mice were used to investigate the pathophysiological role of HIF-2α in MASLD. Multiple gain- and loss-of-function experiments in primary hepatocytes and established human hepatocyte cell lines were performed to elucidate the molecular mechanisms by which HIF-2α contributes to MASLD progression.</div></div><div><h3>Results</h3><div>Compared with their wild-type littermates, hepatocyte-specific HIF-2α knockout mice exhibited a substantial reduction in high-fat diet-induced hepatic steatosis and inflammatory signaling. Furthermore, HIF-2ɑ deficiency in primary hepatocytes and both L02 and MIHA cell lines markedly inhibited the lipid accumulation, inflammation, and endoplasmic reticulum stress in vitro upon free fatty acids challenge. Mechanistically, HIF-2 directly bound to the promoter region of protein kinase RNA-like ER kinase, leading to the activation of the activating transcription factor 4 signaling under metabolic stress, thereby aggravating lipogenesis while inhibiting lipid oxidation in hepatocytes.</div></div><div><h3>Conclusions</h3><div>These data indicate that HIF-2α acts as a contributing factor to MASLD progression via activating transcription factor 4 signaling.</div></div>","PeriodicalId":55974,"journal":{"name":"Cellular and Molecular Gastroenterology and Hepatology","volume":"20 2","pages":"Article 101651"},"PeriodicalIF":7.1,"publicationDate":"2025-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145208189","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"How First Foods Promote Intestinal Epithelial Maturation: Lessons Learned From Suckling Rabbits","authors":"Vanesa Muncan","doi":"10.1016/j.jcmgh.2025.101649","DOIUrl":"10.1016/j.jcmgh.2025.101649","url":null,"abstract":"","PeriodicalId":55974,"journal":{"name":"Cellular and Molecular Gastroenterology and Hepatology","volume":"20 1","pages":"Article 101649"},"PeriodicalIF":7.1,"publicationDate":"2025-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145208313","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Etomidate Improves Antitumor Immunity by Suppressing PD-L1 Expression in Hepatocellular Carcinoma Cells","authors":"Jiali Xu ,&nbsp;Qing Ji ,&nbsp;Yining Chen ,&nbsp;Yu Xu ,&nbsp;Zhihui Wang ,&nbsp;Zhenyu Yuan ,&nbsp;Dapeng Gao ,&nbsp;Lidong Zhang ,&nbsp;Cunming Liu ,&nbsp;Qing Li ,&nbsp;Liren Zhang ,&nbsp;Jingjing Dai","doi":"10.1016/j.jcmgh.2025.101652","DOIUrl":"10.1016/j.jcmgh.2025.101652","url":null,"abstract":"<div><h3>Background &amp; Aims</h3><div>Etomidate, a prevalent intravenous anesthetic agent, has been implicated in the attenuation of tumorigenesis. Our recent investigations elucidated its capacity to impede the malignant progression of hepatocellular carcinoma (HCC). This study aims to elucidate how etomidate modulates the immunosuppressive tumor microenvironment in HCC.</div></div><div><h3>Methods</h3><div>To investigate the multifaceted effects and underlying molecular mechanisms of etomidate, we employed an integrative approach encompassing in vitro and in vivo systems, including patient-derived HCC organoids, 3-dimensional co-culture platforms, patient-derived xenografts, and orthotopic HCC models. A suite of advanced methodologies such as single-cell cytometry by time-of-flight (CyTOF), multiplex immunohistochemistry, and flow cytometric analyses were applied.</div></div><div><h3>Results</h3><div>Our data reveal that etomidate suppresses programmed death-ligand 1 (PD-L1) expression in HCC cells, thereby potentiating antitumor immunity. Mechanistically, etomidate inhibits the Janus kinase 2/signal transducer and activator of transcription 3 axis in tumor cells, leading to reduced <em>PD-L1</em> transcription and increased infiltration and activation of cytotoxic CD8⁺ T lymphocytes.</div></div><div><h3>Conclusions</h3><div>These findings support the hypothesis that etomidate enhances antitumor immunity and boosts the therapeutic efficacy of immune checkpoint blockade, thereby laying a theoretical foundation for precision immunotherapy in HCC.</div></div>","PeriodicalId":55974,"journal":{"name":"Cellular and Molecular Gastroenterology and Hepatology","volume":"20 2","pages":"Article 101652"},"PeriodicalIF":7.1,"publicationDate":"2025-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145208196","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anesthetic Agents as Modulators of Antitumor Immunity: Repurposing Etomidate for Hepatocellular Carcinoma Therapy.","authors":"Hanchao Lin, Qiongzhu Dong","doi":"10.1016/j.jcmgh.2025.101650","DOIUrl":"10.1016/j.jcmgh.2025.101650","url":null,"abstract":"","PeriodicalId":55974,"journal":{"name":"Cellular and Molecular Gastroenterology and Hepatology","volume":" ","pages":"101650"},"PeriodicalIF":7.1,"publicationDate":"2025-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145208129","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cell Adhesion Molecule 1 Emerges as a Biomarker and Therapeutic Opportunity in Inflammatory Bowel Disease","authors":"Randy S. Longman","doi":"10.1016/j.jcmgh.2025.101648","DOIUrl":"10.1016/j.jcmgh.2025.101648","url":null,"abstract":"","PeriodicalId":55974,"journal":{"name":"Cellular and Molecular Gastroenterology and Hepatology","volume":"20 1","pages":"Article 101648"},"PeriodicalIF":7.1,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145187593","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"R-Spondin1 Regulates Fate of Enteric Neural Progenitors via Differential LGR4/5/6 Expression in Mice and Humans","authors":"Melanie Scharr ,&nbsp;Simon Scherer ,&nbsp;Jörg Fuchs ,&nbsp;Bernhard Hirt ,&nbsp;Peter H. Neckel","doi":"10.1016/j.jcmgh.2025.101642","DOIUrl":"10.1016/j.jcmgh.2025.101642","url":null,"abstract":"<div><h3>Background &amp; Aims</h3><div>Regeneration and cytodifferentiation of various adult epithelial stem cell compartments are controlled by the WNT agonist R-Spondin1 (RSPO1) and the Leucin-rich-repeat-containing G-protein-coupled receptors (LGR4/5/6). We hypothesized that RSPO1-LGR signaling is also involved in regulating neuroregeneration and homeostasis of the postnatal enteric nervous system (ENS).</div></div><div><h3>Methods</h3><div>We isolated neural crest-derived ENS cells from wnt1-tomato mice and patient samples, which were evaluated using pharmacological in vitro studies under RSPO1 stimulation. We use proliferation assays (BrdU incorporation, Ki67 staining), as well as neuronal differentiation screenings. We performed fluorescence-activated cell sorting-based in vitro assays to stratify human ENS cells for LGR receptor expression, and to characterize them by immunofluorescence colabeling studies in vivo.</div></div><div><h3>Results</h3><div>If applied to murine and human ENS progenitors, RSPO1 led to an increased proliferation (<em>P</em> = .002), followed by enhanced enteric neurogenesis (<em>P</em> &lt; .001). This coincided with an upregulation of LGR4 expression during ENS progenitor proliferation (<em>P ≤</em> .001) in vitro. In contrast, we observed a reduced proliferation in ENS progenitors expressing LGR5 (<em>P</em> ≤ .001), whereas LGR6 was not expressed by proliferative ENS progenitors (<em>P</em> ≤ .05). Instead, LGR5 and LGR6 expression increased over the course of induced neuronal differentiation (LGR5: <em>P</em> ≤ .001 and LGR6: <em>P</em> ≤ .05), consistent with the in vivo expression.</div></div><div><h3>Conclusions</h3><div>LGR receptor expression therefore might represent a previously unknown mechanism influencing the fate decision of ENS progenitor cells between proliferation and neuronal differentiation. Thus, our study is essential for our understanding of regenerative aspects of the postnatal ENS in health and disease.</div></div>","PeriodicalId":55974,"journal":{"name":"Cellular and Molecular Gastroenterology and Hepatology","volume":"20 2","pages":"Article 101642"},"PeriodicalIF":7.1,"publicationDate":"2025-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145152129","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}