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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 : 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
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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 : 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
K+ Flux Capacitor: NKCC1-mediated Potassium Flow Prevents an Inflammatory Overload. K+通量电容器：nkcc1介导的钾流可防止炎症过载。
IF 7.1 1区 医学 Q1 GASTROENTEROLOGY & HEPATOLOGY
Cellular and Molecular Gastroenterology and Hepatology
Pub Date : 2025-12-01 DOI: 10.1016/j.jcmgh.2025.101696
Noah R Martin, Gregory D Fairn
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引用次数: 0
Mechanistic Insights Driving Translational Progress in Pancreatic Cancer. 驱动胰腺癌转化进展的机制见解。
IF 7.1 1区 医学 Q1 GASTROENTEROLOGY & HEPATOLOGY
Cellular and Molecular Gastroenterology and Hepatology
Pub Date : 2025-11-19 DOI: 10.1016/j.jcmgh.2025.101685
Lincoln N Strickland, Kelsey A Klute, Jennifer M Bailey-Lundberg
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引用次数: 0
Loss of Intestinal Endosome-associated Protein Sorting Nexin 27 Disrupts Epithelial Barrier and Promotes Inflammation 肠内小体相关蛋白分选连接蛋白27的缺失破坏上皮屏障并促进炎症。
IF 7.1 1区 医学 Q1 GASTROENTEROLOGY & HEPATOLOGY
Cellular and Molecular Gastroenterology and Hepatology
Pub Date : 2025-11-17 DOI: 10.1016/j.jcmgh.2025.101682
Shreya Deb , Yongguo Zhang , Yueqing An , Yinglin Xia , Jun Sun

Backgrounds & Aims

SNX27, member of the sorting nexin (SNX) family, carries a unique PDZ domain and mediates recycling of endocytosed transmembrane proteins. SNX27 is critical for neurodevelopmental processes; however, its role in intestine remains unexplored. We aim to determine the previously unknown roles of SNX27 in regulating intestinal homeostasis, epithelial barrier integrity, and inflammatory responses.

Methods

We used available National Center for Biotechnology Information Gene Expression Omnibus and single-cell RNA sequencing datasets to analyze SNX27 expression in human inflammatory bowel disease (IBD). We generated a novel mouse model of SNX27 conditional deletion from intestinal epithelial cells (SNX27ΔIEC) and challenged these mice with dextran sulfate sodium (DSS).

Results

SNX27 expression was significantly lower in human IBD, including ulcerative colitis (UC) and Crohn’s disease (CD). SNX27ΔIEC mice had significantly lower bodyweight and exhibited increased proliferation and poor differentiation of secretory Paneth and goblet cells. We found reduced mucin layer and downregulation of crucial epithelial barrier proteins β-catenin, E-cadherin, ZO-1, ZO-2, and Claudin10 in SNX27ΔIEC mice. SNX27ΔIEC mice showed high intestinal permeability and spontaneously developed intestinal inflammation. Moreover, SNX27ΔIEC mice were more susceptible towards DSS-induced colitis, compared with the SNX27Loxp mice.

Conclusions

Overall, deletion of intestinal epithelial SNX27 weakens barrier functions and promotes inflammation. Our results indicate a novel role of SNX27 in regulating intestinal physiology and protecting against intestinal disorders. Thus, understanding the mechanisms of SNX27 downregulation in IBD will provide insights into new prevention and targets against chronic inflammation.
背景和目的：SNX27是分类连接蛋白（SNX）家族的成员，携带独特的PDZ结构域并介导内吞跨膜蛋白的再循环。SNX27对神经发育过程至关重要，但其在肠道中的作用仍未被探索。我们的目标是确定SNX27在调节肠道稳态、上皮屏障完整性和炎症反应中的未知作用。方法：利用现有的NCBI GEO和单细胞RNA测序数据集分析SNX27在人IBD中的表达。我们从肠上皮细胞中建立了一种新的SNX27条件缺失小鼠模型（SNX27ΔIEC），并用葡聚糖硫酸钠（DSS）刺激这些小鼠。结果：SNX27在包括UC和CD在内的人IBD中表达显著降低，SNX27ΔIEC小鼠体重显著降低，分泌Paneth和Goblet细胞增殖增加，分化差。我们发现SNX27ΔIEC小鼠的粘蛋白层减少，关键上皮屏障蛋白β-catenin、E-cadherin、ZO-1、ZO-2和Claudin10下调。SNX27ΔIEC小鼠表现出高肠通透性并自发发生肠道炎症。此外，与SNX27Loxp小鼠相比，SNX27ΔIEC小鼠更容易患dss诱导的结肠炎。结论：总体而言，肠上皮SNX27的缺失削弱了屏障功能，促进了炎症。我们的研究结果表明SNX27在调节肠道生理和预防肠道疾病方面具有新的作用。因此，了解SNX27在IBD中的下调机制将为新的慢性炎症预防和靶点提供见解。
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引用次数: 0
When BRG1 Turns Off: Chromatin Remodeling and YAP Signaling Drive ITPN Progression. 当BRG1关闭：染色质重塑和YAP信号驱动ITPN进展。
IF 7.1 1区 医学 Q1 GASTROENTEROLOGY & HEPATOLOGY
Cellular and Molecular Gastroenterology and Hepatology
Pub Date : 2025-11-13 DOI: 10.1016/j.jcmgh.2025.101676
Shigetsugu Takano, Masayuki Ohtsuka
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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 : 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
ATG16L1 Regulates Reparative Function of Peritoneal Macrophages During Acute Drug-induced Liver Injury ATG16L1调控急性药物性肝损伤时腹腔巨噬细胞的修复功能。
IF 7.1 1区 医学 Q1 GASTROENTEROLOGY & HEPATOLOGY
Cellular and Molecular Gastroenterology and Hepatology
Pub Date : 2025-11-04 DOI: 10.1016/j.jcmgh.2025.101674
Xun Wang , Xinyu Zhan , Yiyun Gao , Hao Wang , Zheng Liu , Mu Liu , Ling Lu , Haoming Zhou

Background & Aims

Acute drug-induced liver injury (DILI) is a major cause of acute liver dysfunction and even liver failure. Peritoneal macrophages have been reported to invade into the injured liver for tissue repair. Herein, we aimed to investigate the role of autophagy-related 16 like 1 gene (ATG16L1) in regulating the reparative function of peritoneal macrophages during DILI caused by acetaminophen (APAP).

Methods

Myeloid ATG16L1 knockout (KO), overexpression (KI) or wild-type (WT) mice were challenged with a single dose of intraperitoneal APAP (300 mg/kg) injection. Intraperitoneal injection or depletion of peritoneal macrophages was conducted for the in vivo analysis. Co-culture of primary hepatocytes and peritoneal macrophages were applied for in vitro analysis.

Results

Peritoneal macrophages were able to rapidly invade into the liver in response to DILI. Peritoneal macrophage injection promoted, and peritoneal macrophage depletion impaired the resolution of inflammation and liver repair post DILI. DILI triggered ATG16L1 expression in intrahepatic accumulated peritoneal macrophages. Interestingly, compared with WT or KI peritoneal macrophages, KO peritoneal macrophages showed enhanced intrahepatic migration ability via Schlafen family member 5 (SLFN5)-CD44 signaling pathway, leading to less injury at early time of 24 hours post DILI in mice with KO peritoneal macrophage infusion. In addition, ATG16L1-mediated autophagy promoted phagocytosis and reparative phenotype of peritoneal macrophages by regulating reactive oxygen species (ROS)-Mer tyrosine kinase (MerTK) signaling. Moreover, peritoneal macrophage ATG16L1 promoted hepatocyte proliferation dependent on the interleukin (IL)-10–C-X-C motif chemokine receptor 2 (CXCR2) axis.

Conclusions

ATG16L1 activation enhanced peritoneal macrophage phagocytosis and reparative phenotype via autophagy-ROS-MerTK signaling and promoted IL-10-CXCR2-dependent hepatocyte proliferation during DILI. Peritoneal macrophage ATG16L1 might be a novel therapeutic target for DILI.
背景与目的：急性药物性肝损伤（Acute drug-induced liver injury， DILI）是引起急性肝功能障碍甚至肝功能衰竭的主要原因。据报道，腹膜巨噬细胞侵入损伤的肝脏进行组织修复。在此，我们旨在研究ATG16L1在对乙酰氨基酚（APAP）引起的DILI中调节腹腔巨噬细胞修复功能的作用。方法：用单剂量APAP （300 mg/kg）腹腔注射ATG16L1敲除（KO）、过表达（KI）或野生型（WT）小鼠。通过腹腔注射或腹腔巨噬细胞清除进行体内分析。体外分析采用原代肝细胞与腹腔巨噬细胞共培养。结果：腹腔巨噬细胞对DILI反应迅速侵入肝脏。腹腔巨噬细胞注射促进了DILI后炎症的消退和肝脏修复，腹腔巨噬细胞缺失损害了DILI后炎症的消退和肝脏修复。DILI触发肝内积聚的腹腔巨噬细胞中ATG16L1的表达。有趣的是，与WT或KI腹膜巨噬细胞相比，KO腹膜巨噬细胞通过SLFN5-CD44信号通路表现出更强的肝内迁移能力，导致KO腹膜巨噬细胞输注小鼠DILI后24h早期损伤较小。此外，atg16l1介导的自噬通过调节ROS-MerTK信号通路促进吞噬和腹腔巨噬细胞的修复表型。此外，腹腔巨噬细胞ATG16L1通过IL-10-CXCR2轴促进肝细胞增殖。结论：ATG16L1激活可通过自噬- ros - mertk信号增强腹腔巨噬细胞吞噬和修复表型，促进DILI期间il -10- cxcr2依赖性肝细胞增殖。腹腔巨噬细胞ATG16L1可能是DILI的一个新的治疗靶点。
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引用次数: 0
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 : 2025-11-04 DOI: 10.1016/j.jcmgh.2025.101675
Beatriz Thomasi
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引用次数: 0
VCAM-1 and Osteopontin Link Hemodynamic Alteration to Fibrosis in Portal Hypertension. VCAM-1和骨桥蛋白与门脉高压症纤维化的血流动力学改变有关。
IF 7.1 1区 医学 Q1 GASTROENTEROLOGY & HEPATOLOGY
Cellular and Molecular Gastroenterology and Hepatology
Pub Date : 2025-10-21 DOI: 10.1016/j.jcmgh.2025.101663
Akitoshi Sano, Qianqian Guo, Samar H Ibrahim
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引用次数: 0
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