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Gut Feelings Get Intense Due to Early Life Stress and Immune Imbalance 由于早年的生活压力和免疫失衡，直觉会变得强烈。
IF 7.1 1区 医学 Q1 GASTROENTEROLOGY & HEPATOLOGY
Cellular and Molecular Gastroenterology and Hepatology
Pub Date : 2026-01-01 Epub Date: 2025-11-04 DOI: 10.1016/j.jcmgh.2025.101675
Beatriz Thomasi
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引用次数: 0
Distinct chronic Pancreatitis Genetic Variants CPA1 N256K and PNLIP T221M Share Common Pathological Grounds 不同的慢性胰腺炎遗传变异CPA1 N256K和PNLIP T221具有共同的病理基础。
IF 7.1 1区 医学 Q1 GASTROENTEROLOGY & HEPATOLOGY
Cellular and Molecular Gastroenterology and Hepatology
Pub Date : 2026-01-01 Epub Date: 2025-11-13 DOI: 10.1016/j.jcmgh.2025.101677
Michelle M. Cooley , Guy E. Groblewski
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引用次数: 0
Storage Wars: Adipose-liver Crosstalk as a Determinant of Liver Injury 储存之战：脂肪-肝脏串扰是肝损伤的决定因素。
IF 7.1 1区 医学 Q1 GASTROENTEROLOGY & HEPATOLOGY
Cellular and Molecular Gastroenterology and Hepatology
Pub Date : 2026-01-01 Epub Date: 2025-12-01 DOI: 10.1016/j.jcmgh.2025.101700
Abigail E. Russi, Brian J. DeBosch
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引用次数: 0
Unlocking the Neurogenic Potential of Enteric Glial Cells for Hirschsprung Disease Therapy 解锁肠胶质细胞治疗先天性巨结肠疾病的神经发生潜能。
IF 7.1 1区 医学 Q1 GASTROENTEROLOGY & HEPATOLOGY
Cellular and Molecular Gastroenterology and Hepatology
Pub Date : 2026-01-01 Epub Date: 2025-12-01 DOI: 10.1016/j.jcmgh.2025.101693
Klaas Van Mechelen, Jing Zhao, Madeleine R. Di Natale, Linxuan Jiang, David K. Lai, Hui Yu, Matilde Oviedo Querejazu, John B. Furness, Pieter Vanden Berghe, Marlene M. Hao, Lincon A. Stamp
{"title":"Unlocking the Neurogenic Potential of Enteric Glial Cells for Hirschsprung Disease Therapy","authors":"Klaas Van Mechelen, Jing Zhao, Madeleine R. Di Natale, Linxuan Jiang, David K. Lai, Hui Yu, Matilde Oviedo Querejazu, John B. Furness, Pieter Vanden Berghe, Marlene M. Hao, Lincon A. Stamp","doi":"10.1016/j.jcmgh.2025.101693","DOIUrl":"10.1016/j.jcmgh.2025.101693","url":null,"abstract":"","PeriodicalId":55974,"journal":{"name":"Cellular and Molecular Gastroenterology and Hepatology","volume":"20 5","pages":"Article 101693"},"PeriodicalIF":7.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145671193","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}
引用次数: 0
The Intestinal Cues Promoting Serotonin Release From the Human Gut 肠道信号促进人体肠道释放血清素。
IF 7.1 1区 医学 Q1 GASTROENTEROLOGY & HEPATOLOGY
Cellular and Molecular Gastroenterology and Hepatology
Pub Date : 2026-01-01 Epub Date: 2025-10-18 DOI: 10.1016/j.jcmgh.2025.101664
Sara C. Di Rienzi
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引用次数: 0
Serum Amyloid A Protein Promotes Fibrolysis and Recovery Following Alcohol Withdrawal. SAA促进酒精戒断后的纤维溶解和恢复。
IF 7.1 1区 医学 Q1 GASTROENTEROLOGY & HEPATOLOGY
Cellular and Molecular Gastroenterology and Hepatology
Pub Date : 2026-01-01 Epub Date: 2026-01-16 DOI: 10.1016/j.jcmgh.2026.101726
Jessica L Maiers
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引用次数: 0
Introducing Advocacy and Impact Section. 介绍宣传和影响科。
IF 7.1 1区 医学 Q1 GASTROENTEROLOGY & HEPATOLOGY
Cellular and Molecular Gastroenterology and Hepatology
Pub Date : 2026-01-01 Epub Date: 2025-12-15 DOI: 10.1016/j.jcmgh.2025.101692
Vivian Ortiz
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引用次数: 0
Microbiota Regulation of Duodenal Adenoma Development: Bile Acids Join the Team. 微生物群调控十二指肠腺瘤的发展：胆汁酸加入团队。
IF 7.1 1区 医学 Q1 GASTROENTEROLOGY & HEPATOLOGY
Cellular and Molecular Gastroenterology and Hepatology
Pub Date : 2026-01-01 Epub Date: 2026-01-24 DOI: 10.1016/j.jcmgh.2026.101738
Wenjing Yang, Yingzi Cong
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引用次数: 0
Macrophage Nogo-B Drives Liver Fibrosis 巨噬细胞Nogo-B驱动肝纤维化。
IF 7.1 1区 医学 Q1 GASTROENTEROLOGY & HEPATOLOGY
Cellular and Molecular Gastroenterology and Hepatology
Pub Date : 2026-01-01 Epub Date: 2025-09-02 DOI: 10.1016/j.jcmgh.2025.101622
Lei Zhang , Ming Ni , Jiahao Si , Feng Cheng , Long Zhang , Yuan Liang , Mu Liu , Wenzhu Li , Junda Li , Yongquan Chi , Jianhua Rao , Ling Lu

Background & Aims

Liver fibrosis is characterized by sustained injury stress, chronic inflammation, and repeated cell death and repair, all of which promote the progression of end-stage liver diseases (eg, liver cirrhosis and carcinoma). As an endoplasmic reticulum-residential protein, Nogo-B strongly regulates macrophage function, but whether Nogo-B-decorated macrophages affect inflammation and progression during liver fibrosis is unclear. The purpose of our current study was to elucidate the roles of Nogo-Bhigh macrophages during liver fibrosis development.

Methods

The expression and distribution of Nogo-B were analyzed in clinical specimens and animal models. By utilizing myeloid-specific Nogo-B knockout (Nogo-Bmko) mice, the mechanism and functionality of Nogo-Bhigh macrophages were investigated in 3 murine liver fibrosis models, which were induced separately by bile duct ligation, methionine- and choline-deficient diets, and carbon tetrachloride administration.

Results

Our study revealed the predominant expression of Nogo-B in fibrotic liver macrophages and its positive correlation with fibrosis stage. Myeloid-specific Nogo-B deficiency effectively alleviated liver inflammation, injury, and fibrosis in 3 liver fibrosis models. Importantly, Nogo-B deficiency inhibited NOD-like receptor protein 3 (NLRP3) inflammasome activation and necroptosis in macrophages both in vivo and in vitro. Notably, receptor-interacting serine-threonine kinase 3 (RIPK3) is vital for Nogo-B-driven NLRP3 inflammasome activation and necroptosis in macrophages. Additionally, adoptive transfer of macrophages revealed that the Nogo-B/RIPK3 axis promoted NLRP3 inflammasome activation and necroptosis and accelerated liver fibrosis. Mechanistically, Nogo-B-mediated recruitment of ubiquitin-specific protease 14 restricted the degree of RIPK3 ubiquitination and increased RIPK3 stabilization.

Conclusions

Nogo-B facilitates liver fibrosis by recruiting the deubiquitination enzyme USP14, which increases the stabilization of RIPK3 and promotes NLRP3 inflammasome activation and necroptosis in macrophages.
背景与目的：肝纤维化的特点是持续的损伤应激、慢性炎症和反复的细胞死亡和修复，所有这些都促进了终末期肝病（如肝硬化和肝癌）的进展。作为一种内质网驻留蛋白，Nogo-B强烈调节巨噬细胞功能，但Nogo-B修饰的巨噬细胞是否影响肝纤维化期间的炎症和进展尚不清楚。我们当前研究的目的是阐明Nogo-Bhigh巨噬细胞在肝纤维化发展中的作用。方法：分析Nogo-B在临床标本和动物模型中的表达和分布。利用骨髓特异性Nogo-B敲除（Nogo-Bmko）小鼠，研究了Nogo-B高巨噬细胞在胆管结联（BDL）、蛋氨酸和胆碱缺乏（MCD）饮食和四氯化碳（CCl4）诱导的3种小鼠肝纤维化模型中的作用机制和功能。结果：Nogo-B在肝纤维化巨噬细胞中显著表达，并与纤维化分期呈正相关。骨髓特异性Nogo-B缺乏可有效减轻三种肝纤维化模型的肝脏炎症、损伤和纤维化。重要的是，在体内和体外，Nogo-B缺乏均抑制了巨噬细胞NLRP3炎性体的激活和坏死性凋亡。值得注意的是，RIPK3对于巨噬细胞中nogo - b驱动的NLRP3炎症小体激活和坏死坏死至关重要。此外，巨噬细胞过继性转移显示，Nogo-B/RIPK3轴促进NLRP3炎性体活化和坏死坏死，加速肝纤维化。在机制上，nogo - b介导的USP14的募集限制了RIPK3泛素化的程度，增加了RIPK3的稳定性。结论：Nogo-B通过募集去泛素化酶USP14促进肝纤维化，增加RIPK3的稳定性，促进巨噬细胞NLRP3炎性体活化和坏死坏死。
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引用次数: 0
Supporting the Scientists Behind the Science 支持科学背后的科学家。
IF 7.1 1区 医学 Q1 GASTROENTEROLOGY & HEPATOLOGY
Cellular and Molecular Gastroenterology and Hepatology
Pub Date : 2026-01-01 Epub Date: 2025-12-16 DOI: 10.1016/j.jcmgh.2025.101691
Jonathan P. Katz, Michele A. Battle
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引用次数: 0
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