Cellular and Molecular Gastroenterology and Hepatology最新文献

{"title":"Tolerogenic pDCs Turn the Inflammatory Tide and Protect Against Acute Liver Failure","authors":"","doi":"10.1016/j.jcmgh.2024.101370","DOIUrl":"10.1016/j.jcmgh.2024.101370","url":null,"abstract":"","PeriodicalId":55974,"journal":{"name":"Cellular and Molecular Gastroenterology and Hepatology","volume":"18 3","pages":"Article 101370"},"PeriodicalIF":7.1,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2352345X24001255/pdfft?md5=62294a2f6607114fbe2c85c1cc957a87&pid=1-s2.0-S2352345X24001255-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141592239","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cover","authors":"","doi":"10.1016/S2352-345X(24)00151-6","DOIUrl":"10.1016/S2352-345X(24)00151-6","url":null,"abstract":"","PeriodicalId":55974,"journal":{"name":"Cellular and Molecular Gastroenterology and Hepatology","volume":"18 4","pages":"Article 101396"},"PeriodicalIF":7.1,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2352345X24001516/pdfft?md5=f69a8da5f1bd8fbfe178866795f93d73&pid=1-s2.0-S2352345X24001516-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142239831","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"BRD4 Regulates Glycolysis-Dependent Nos2 Expression in Macrophages Upon H pylori Infection","authors":"Nikita Modi ,&nbsp;Yanheng Chen ,&nbsp;Xingchen Dong ,&nbsp;Xiangming Hu ,&nbsp;Gee W. Lau ,&nbsp;Keith T. Wilson ,&nbsp;Richard M. Peek Jr. ,&nbsp;Lin-Feng Chen","doi":"10.1016/j.jcmgh.2023.10.001","DOIUrl":"10.1016/j.jcmgh.2023.10.001","url":null,"abstract":"<div><h3>Background &amp; Aims</h3><p>Metabolic reprogramming is essential for the activation and functions of macrophages, including bacterial killing and cytokine production. Bromodomain-containing protein 4 (BRD4) has emerged as a critical regulator of innate immune response. However, the potential role of BRD4 in the metabolic reprogramming of macrophage activation upon <em>Helicobacter pylori</em> infection remains unclear.</p></div><div><h3>Methods</h3><p>Bone marrow–derived macrophages (BMDMs) from wild-type (WT) and <em>Brd4-</em>myeloid deletion conditional knockout (<em>Brd4</em>-CKO) mice were infected with <em>H pylori</em>. RNA sequencing was performed to evaluate the differential gene expression between WT and <em>Brd4</em>-deficient BMDMs upon infection. An in vivo model of <em>H pylori</em> infection using WT and <em>Brd4</em>-CKO mice was used to confirm the role of BRD4 in innate immune response to infection.</p></div><div><h3>Results</h3><p>Depletion of <em>Brd4</em> in BMDMs showed impaired <em>H pylori</em>–induced glycolysis. In addition, <em>H pylori</em>–induced expression of glycolytic genes, including <em>Slc2a1</em> and <em>Hk2</em>, was decreased in <em>Brd4</em>-deficient BMDMs. BRD4 was recruited to the promoters of <em>Slc2a1</em> and <em>Hk2</em> via hypoxia-inducible factor-1α, facilitating their expression. BRD4-mediated glycolysis stabilized <em>H pylori</em>–induced nitric oxide synthase (<em>Nos2</em>) messenger RNA to produce nitric oxide. The NO-mediated killing of <em>H pylori</em> decreased in <em>Brd4</em>-deficient BMDMs, which was rescued by pyruvate. Furthermore, <em>Brd4</em>-CKO mice infected with <em>H pylori</em> showed reduced gastric inflammation and increased <em>H pylori</em> colonization with reduced inducible NO synthase expression in gastric macrophages.</p></div><div><h3>Conclusions</h3><p>Our study identified BRD4 as a key regulator of hypoxia-inducible factor-1α–dependent glycolysis and macrophage activation. Furthermore, we show a novel regulatory role of BRD4 in innate immunity through glycolysis to stabilize <em>Nos2</em> messenger RNA for NO production to eliminate <em>H pylori</em> infection.</p></div>","PeriodicalId":55974,"journal":{"name":"Cellular and Molecular Gastroenterology and Hepatology","volume":"17 2","pages":"Pages 292-308.e1"},"PeriodicalIF":7.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2352345X23001807/pdfft?md5=040896a362f7f6eaf447d7e1b5a53ee0&pid=1-s2.0-S2352345X23001807-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41221049","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cover","authors":"","doi":"10.1016/S2352-345X(24)00181-4","DOIUrl":"10.1016/S2352-345X(24)00181-4","url":null,"abstract":"","PeriodicalId":55974,"journal":{"name":"Cellular and Molecular Gastroenterology and Hepatology","volume":"18 6","pages":"Article 101426"},"PeriodicalIF":7.1,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142658574","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Th2 Cell Activation in Chronic Liver Disease Is Driven by Local IL33 and Contributes to IL13-Dependent Fibrogenesis","authors":"Johanna Reißing ,&nbsp;Marie Berres ,&nbsp;Pavel Strnad ,&nbsp;Alexander Wree ,&nbsp;Maria Eugenia Inzaugarat ,&nbsp;Christian Trautwein ,&nbsp;Tony Bruns ,&nbsp;Henning Wolfgang Zimmermann","doi":"10.1016/j.jcmgh.2023.12.011","DOIUrl":"10.1016/j.jcmgh.2023.12.011","url":null,"abstract":"<div><h3>Background &amp; Aims</h3><p>Type 2 immune responses contribute to liver fibrosis in parasite infections, but their role in other liver diseases is less well understood. Here, we aimed at unravelling mechanisms involved in T helper 2 (Th2) T-cell polarization, activation, and recruitment in human liver fibrosis and cirrhosis.</p></div><div><h3>Methods</h3><p>Tissues, cells, and serum from human livers were analyzed using quantitative reverse-transcription polymerase chain reaction, enzyme-linked immunosorbent assay, fluorescence in situ hybridization, immunostaining, flow cytometry, and various functional in vitro assays. Cellular interactions and soluble mediators involved in T-cell polarization and recruitment were studied, as well as their effect on hepatic stellate cell (HSC) activation, proliferation, and extracellular matrix synthesis.</p></div><div><h3>Results</h3><p>In human liver fibrosis, a stage-dependent increase in Th2-related transcription factors, Th2 cytokines, and trans-acting T-cell–specific transcription factor–expressing T cells was observed, and was highest in cirrhotic livers. The alarmin interleukin (IL)33 was found to be increased in livers and sera from patients with cirrhosis, to act as a chemotactic agent for Th2 cells, and to induce type 2 polarization of CD4+ T cells. Oval cells, liver sinusoidal endothelial cells, intrahepatic macrophages, and migrating monocytes were identified as sources of IL33. IL33-activated T cells, but not IL33 alone, induced HSC activation, as shown by Ki67 and α-smooth muscle actin staining, increased collagen type I alpha 1 chain messenger RNA expression, and wound healing assays. The profibrotic effect of IL33-activated T cells was contact-independent and could be antagonized using monoclonal antibodies against IL13.</p></div><div><h3>Conclusion</h3><p>In patients with chronic liver disease, the alarmin IL33 promotes the recruitment and activation of CD4+ T cells with Th2-like properties, which activate paracrine HSC in an IL13-dependent manner and promotes fibrogenesis.</p></div>","PeriodicalId":55974,"journal":{"name":"Cellular and Molecular Gastroenterology and Hepatology","volume":"17 4","pages":"Pages 517-538"},"PeriodicalIF":7.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2352345X23002278/pdfft?md5=2e5b8335236214bf8d30b1dc63316401&pid=1-s2.0-S2352345X23002278-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139054066","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Promises and Limitations of Current Models for Understanding Barrett’s Esophagus and Esophageal Adenocarcinoma","authors":"Omar Martinez-Uribe ,&nbsp;Thomas C. Becker ,&nbsp;Katherine S. Garman","doi":"10.1016/j.jcmgh.2024.01.017","DOIUrl":"10.1016/j.jcmgh.2024.01.017","url":null,"abstract":"<div><h3>Background &amp; Aims</h3><p>This review was developed to provide a thorough and effective update on models relevant to esophageal metaplasia, dysplasia, and carcinogenesis, focusing on the advantages and limitations of different models of Barrett’s esophagus (BE) and esophageal adenocarcinoma (EAC).</p></div><div><h3>Methods</h3><p>This expert review was written on the basis of a thorough review of the literature combined with expert interpretation of the state of the field. We emphasized advances over the years 2012–2023 and provided detailed information related to the characterization of established human esophageal cell lines.</p></div><div><h3>Results</h3><p>New insights have been gained into the pathogenesis of BE and EAC using patient-derived samples and single-cell approaches. Relevant animal models include genetic as well as surgical mouse models and emphasize the development of lesions at the squamocolumnar junction in the mouse stomach. Rat models are generated using surgical approaches that directly connect the small intestine and esophagus. Large animal models have the advantage of including features in human esophagus such as esophageal submucosal glands. Alternatively, cell culture approaches remain important in the field and allow for personalized approaches, and scientific rigor can be ensured by authentication of cell lines.</p></div><div><h3>Conclusions</h3><p>Research in BE and EAC remains highly relevant given the morbidity and mortality associated with cancers of the tubular esophagus and gastroesophageal junction. Careful selection of models and inclusion of human samples whenever possible will ensure relevance to human health and disease.</p></div>","PeriodicalId":55974,"journal":{"name":"Cellular and Molecular Gastroenterology and Hepatology","volume":"17 6","pages":"Pages 1025-1038"},"PeriodicalIF":7.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2352345X24000201/pdfft?md5=02615a07a567c8760236e308035da1af&pid=1-s2.0-S2352345X24000201-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139704136","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of ICAM-1 in the Adhesion of T Cells to Enteric Glia: Perspectives in the Formation of Plexitis in Crohn’s Disease","authors":"Julie Pabois ,&nbsp;Tony Durand ,&nbsp;Catherine Le Berre ,&nbsp;Rhiannon T. Filippone ,&nbsp;Théo Noël ,&nbsp;Emilie Durieu ,&nbsp;Céline Bossard ,&nbsp;Sarah Bruneau ,&nbsp;Malvyne Rolli-Derkinderen ,&nbsp;Kulmira Nurgali ,&nbsp;Michel Neunlist ,&nbsp;Arnaud Bourreille ,&nbsp;Isabelle Neveu ,&nbsp;Philippe Naveilhan","doi":"10.1016/j.jcmgh.2024.02.016","DOIUrl":"10.1016/j.jcmgh.2024.02.016","url":null,"abstract":"<div><h3>Background &amp; Aims</h3><p>The presence of myenteric plexitis in the proximal resection margins is a predictive factor of early postoperative recurrence in Crohn’s disease. To decipher the mechanisms leading to their formation, T-cell interactions with enteric neural cells were studied in vitro and in vivo.</p></div><div><h3>Methods</h3><p>T cells close to myenteric neural cells were retrospectively quantified in ileocolonic resections from 9 control subjects with cancer and 20 patients with Crohn’s disease. The mechanisms involved in T-cell adhesion were then investigated in co-cultures of T lymphocytes with enteric glial cells (glia). Finally, the implication of adhesion molecules in the development of plexitis and colitis was studied in vitro but also in vivo in Winnie mice.</p></div><div><h3>Results</h3><p>The mean number of T cells close to glia, but not neurons, was significantly higher in the myenteric ganglia of relapsing patients with Crohn’s disease (2.42 ± 0.5) as compared with controls (0.36 ± 0.08, <em>P</em> = .0007). Co-culture experiments showed that exposure to proinflammatory cytokines enhanced T-cell adhesion to glia and increased intercellular adhesion molecule-1 (ICAM-1) expression in glia. We next demonstrated that T-cell adhesion to glia was inhibited by an anti–ICAM-1 antibody. Finally, using the Winnie mouse model of colitis, we showed that the blockage of ICAM-1/lymphocyte function-associated antigen-1 (LFA-1) with lifitegrast reduced colitis severity and decreased T-cell infiltration in the myenteric plexus.</p></div><div><h3>Conclusions</h3><p>Our present work argues for a role of glia–T-cell interaction in the development of myenteric plexitis through the adhesion molecules ICAM-1/LFA-1 and suggests that deciphering the functional consequences of glia–T-cell interaction is important to understand the mechanisms implicated in the development and recurrence of Crohn’s disease.</p></div>","PeriodicalId":55974,"journal":{"name":"Cellular and Molecular Gastroenterology and Hepatology","volume":"18 1","pages":"Pages 133-153"},"PeriodicalIF":7.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2352345X2400050X/pdfft?md5=da24d11348be30a3d1f546e383c7dccf&pid=1-s2.0-S2352345X2400050X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140013771","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fatty Acid Esterification as a NASH Therapeutic Target","authors":"Ikki Sakuma,&nbsp;Daniel F. Vatner","doi":"10.1016/j.jcmgh.2023.10.011","DOIUrl":"10.1016/j.jcmgh.2023.10.011","url":null,"abstract":"","PeriodicalId":55974,"journal":{"name":"Cellular and Molecular Gastroenterology and Hepatology","volume":"17 2","pages":"Pages 311-312"},"PeriodicalIF":7.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2352345X2300190X/pdfft?md5=2a16e99e77d59699d75db91baafb36f5&pid=1-s2.0-S2352345X2300190X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138178095","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Therapeutic Effect of Proteinase-Activated Receptor-1 Antagonist on Colitis-Associated Carcinogenesis","authors":"Xiaodong Li ,&nbsp;Lin-Hai Kurahara ,&nbsp;Zhixin Zhao ,&nbsp;Feiyan Zhao ,&nbsp;Ryo Ishikawa ,&nbsp;Kiyomi Ohmichi ,&nbsp;Gaopeng Li ,&nbsp;Tetsuo Yamashita ,&nbsp;Takeshi Hashimoto ,&nbsp;Mayumi Hirano ,&nbsp;Zhihong Sun ,&nbsp;Katsuya Hirano","doi":"10.1016/j.jcmgh.2024.04.001","DOIUrl":"10.1016/j.jcmgh.2024.04.001","url":null,"abstract":"<div><h3>Background &amp; Aims</h3><p>Inflammatory bowel disease is associated with carcinogenesis, which limits the prognosis of the patients. The local expression of proteinases and proteinase-activated receptor 1 (PAR₁) increases in inflammatory bowel disease. The present study investigated the therapeutic effects of PAR₁ antagonism on colitis-associated carcinogenesis.</p></div><div><h3>Methods</h3><p>A colitis-associated carcinogenesis model was prepared in mice by treatment with azoxymethane (AOM) and dextran sulfate sodium (DSS). PAR₁ antagonist E5555 was administered in long- and short-term protocol, starting on the day of AOM injection and 1 week after completing AOM/DSS treatment, respectively. The fecal samples were collected for metagenome analysis of gut microbiota. The intestinal myofibroblasts of the Crohn’s disease patients were used to elucidate underlying cellular mechanisms. Caco-2 cells were used to investigate a possible source of PAR₁ agonist proteinases.</p></div><div><h3>Results</h3><p>AOM/DSS model showed weight loss, diarrhea, tumor development, inflammation, fibrosis, and increased production of inflammatory cytokines. The β-diversity, but not α-diversity, of microbiota significantly differed between AOM/DSS and control mice. E5555 alleviated these pathological changes and altered the microbiota β-diversity in AOM/DSS mice. The thrombin expression was up-regulated in tumor and non-tumor areas, whereas PAR₁ mRNA expression was higher in tumor areas compared with non-tumor areas. E5555 inhibited thrombin-triggered elevation of cytosolic Ca²⁺ concentration and ERK1/2 phosphorylation, as well as IL6-induced signal transducer and activator of transcription 3 (STAT3) phosphorylation in intestinal myofibroblasts. Caco-2 cell-conditioned medium contained immunoreactive thrombin, which cleaved the recombinant protein containing the extracellular domain of PAR₁ at the thrombin cleavage site.</p></div><div><h3>Conclusions</h3><p>PAR₁ antagonism is proposed to be a novel therapeutic strategy for treatment of inflammatory bowel disease and its associated carcinogenesis.</p></div>","PeriodicalId":55974,"journal":{"name":"Cellular and Molecular Gastroenterology and Hepatology","volume":"18 1","pages":"Pages 105-131"},"PeriodicalIF":7.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2352345X24000717/pdfft?md5=8b994d1d5ae16166b21f33644cff1753&pid=1-s2.0-S2352345X24000717-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140790423","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Acvr1b Loss Increases Formation of Pancreatic Precancerous Lesions From Acinar and Ductal Cells of Origin","authors":"Kiyoshi Saeki ,&nbsp;Ian S. Wood ,&nbsp;Wei Chuan Kevin Wang ,&nbsp;Shilpa Patil ,&nbsp;Yanping Sun ,&nbsp;David F. Schaeffer ,&nbsp;Gloria H. Su ,&nbsp;Janel L. Kopp","doi":"10.1016/j.jcmgh.2024.101387","DOIUrl":"10.1016/j.jcmgh.2024.101387","url":null,"abstract":"<div><h3>Background &amp; Aims</h3><p>Pancreatic ductal adenocarcinoma can develop from precursor lesions, including pancreatic intraepithelial neoplasia and intraductal papillary mucinous neoplasm (IPMN). Previous studies indicated that loss of <em>Acvr1b</em> accelerates the Kras-mediated development of papillary IPMN in the mouse pancreas; however, the cell type predominantly affected by these genetic changes remains unclear.</p></div><div><h3>Methods</h3><p>We investigated the contribution of cellular origin by inducing IPMN associated mutations (KRAS^G12D expression and <em>Acvr1b</em> loss) specifically in acinar (<em>Ptf1a</em>^{<em>CreER</em>}<em>;Kras</em>^{<em>LSL-G12D</em>}<em>;Acvr1b</em>^{<em>fl/fl</em>} mice) or ductal (<em>Sox9CreER;Kras</em>^{<em>LSL-G12D</em>}<em>;Acvr1b</em>^{<em>fl/fl</em>} mice) cells in mice. We then performed magnetic resonance imaging and a thorough histopathologic analysis of their pancreatic tissues.</p></div><div><h3>Results</h3><p>The loss of <em>Acvr1b</em> increased the development of pancreatic intraepithelial neoplasia and IPMN-like lesions when either acinar or ductal cells expressed a Kras mutation. Magnetic resonance imaging, immunohistochemistry, and histology revealed large IPMN-like lesions in these mice that exhibited features of flat, gastric epithelium. In addition, cyst formation in both mouse models was accompanied by chronic pancreatitis. Experimental acute pancreatitis accelerated the development of large mucinous cysts and pancreatic intraepithelial neoplasia when acinar, but not ductal, cells expressed mutant Kras and lost <em>Acvr1b</em>.</p></div><div><h3>Conclusions</h3><p>These findings indicate that loss of <em>Acvr1b</em> in the presence of the Kras oncogene promotes the development of large and small precancerous lesions from both ductal and acinar cells. However, the IPMN-like phenotype was not equivalent to that observed when these mutations were made in all pancreatic cells during development. Our study underscores the significance of the cellular context in the initiation and progression of precursor lesions from exocrine cells.</p></div>","PeriodicalId":55974,"journal":{"name":"Cellular and Molecular Gastroenterology and Hepatology","volume":"18 5","pages":"Article 101387"},"PeriodicalIF":7.1,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2352345X24001425/pdfft?md5=ff59ce20a13fca8c0be9687f86fc11bd&pid=1-s2.0-S2352345X24001425-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141903656","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}