CMGH is the newest peer-reviewed journal published by the American Gastroenterological Association (AGA), joining Gastroenterology and Clinical Gastroenterology and Hepatology. The mission of CMGH is to publish impactful digestive biology research that ranges from mechanisms of normal function to pathobiology and covers a broad spectrum of themes in gastroenterology, hepatology, and pancreatology. The journal reports the latest advances in cell biology, immunology, physiology, microbiology, genetics, and neurobiology of gastrointestinal, hepatobiliary, and pancreatic health and disease. The research CMGH publishes is hypothesis driven, mechanistically novel, and appropriately designed and powered. Studies published in CMGH address important questions using tissues or cells from patients or animal models in order to make fundamental discoveries and translate them to human disease.

CMGH is the newest peer-reviewed journal published by the American Gastroenterological Association (AGA), joining Gastroenterology and Clinical Gastroenterology and Hepatology. The mission of CMGH is to publish impactful research in digestive biology, covering a wide range of themes from the mechanisms of normal function to pathobiology in gastroenterology, hepatology, and pancreatology. The journal reports the latest advances in cell biology, immunology, physiology, microbiology, genetics, and neurobiology related to gastrointestinal, hepatobiliary, and pancreatic health and disease. The research published in CMGH is hypothesis-driven, mechanistically novel, and appropriately designed and powered. Studies published in CMGH address significant questions using tissues or cells from patients or animal models to make fundamental discoveries and translate them into human disease.

CMGH是由美国胃肠病学会（AGA）最新出版的同行评审期刊，加入了《Gastroenterology》和《Clinical Gastroenterology and Hepatology》。CMGH的使命是发表具有影响力的消化生物学研究，涵盖从正常功能机制到病理生物学的广泛主题，涉及胃肠病学、肝病学和胰腺病学。期刊报道了细胞生物学、免疫学、生理学、微生物学、遗传学和神经生物学在胃肠、肝胆和胰腺健康与疾病中的最新进展。CMGH发表的研究是以假设为驱动，具有机制新颖性，并经过适当设计和有足够的样本量。发表在CMGH上的研究解决了重要问题，使用来自患者或动物模型的组织或细胞，以便进行基础发现并将其转化为人类疾病的研究。

CMGH

Arthur J. Kastl

Natalie A. Terry

Gary D Wu

Lindsey G. Albenberg

Cellular and Molecular Gastroenterology and Hepatology

The Structure and Function of the Human Small Intestinal Microbiota: Current Understanding and Future Directions

人类小肠微生物群的结构与功能：当前认知与未来方向

Transforming growth factor-β1 (TGF-β1) plays important roles in chronic liver diseases, including metabolic dysfunction-associated steatotic liver disease (MASLD). MASLD involves various biological processes including dysfunctional cholesterol metabolism and contributes to progression to metabolic dysfunction-associated steatohepatitis and hepatocellular carcinoma. However, the reciprocal regulation of TGF-β1 signaling and cholesterol metabolism in MASLD is yet unknown.

Sai Wang

Frederik Link

Mei Han

Roohi Chaudhary

Anastasia Asimakopoulos

Roman Liebe

Ye Yao

Seddik Hammad

Anne Dropmann

Marinela Krizanac

Claudia Rubie

Laura Kim Feiner

Matthias Glanemann

Matthias P A Ebert

Ralf Weiskirchen

Yoav I Henis

Marcelo Ehrlich

Steven Dooley

Cellular and molecular gastroenterology and hepatology

Cell Mol Gastroenterol Hepatol

The Interplay of TGF-β1 and Cholesterol Orchestrating Hepatocyte Cell Fate, EMT, and Signals for HSC Activation.

TGF-β1与胆固醇的相互作用调控肝细胞命运、上皮间质转化及肝星状细胞激活信号。

Every year, enteric infections and associated diarrhea kill millions of people. The situation is compounded by increases in the number of enteric pathogens that are acquiring resistance to antibiotics, as well as (hitherto) a relative paucity of information on host molecular targets that may contribute to diarrhea. Many forms of diarrheal disease depend on the dysregulation of intestinal ion transporters, and an associated imbalance between secretory and absorptive functions of the intestinal epithelium. A number of major transporters have been implicated in the pathogenesis of diarrheal diseases and thus an understanding of their expression, localization, and regulation after infection with various bacteria, viruses, and protozoa likely will prove critical in designing new therapies. This article surveys our understanding of transporters that are modulated by specific pathogens and the mechanism(s) involved, thereby illuminating targets that might be exploited for new therapeutic approaches.

Soumita Das

Rashini Jayaratne

Kim E. Barrett

The Role of Ion Transporters in the Pathophysiology of Infectious Diarrhea

离子转运体在感染性腹泻病理生理学中的作用

Food additives, such as emulsifiers, stabilizers, or bulking agents, are present in the Western diet and their consumption is increasing. However, little is known about their potential effects on intestinal homeostasis. In this study we examined the effect of some of these food additives on gut inflammation.Mice were given drinking water containing maltodextrin (MDX), propylene glycol, or animal gelatin, and then challenged with dextran sulfate sodium or indomethacin. In parallel, mice fed a MDX-enriched diet were given the endoplasmic reticulum (ER) stress inhibitor tauroursodeoxycholic acid (TUDCA). Transcriptomic analysis, real-time polymerase chain reaction, mucin-2 expression, phosphorylated p38 mitogen-activated protein (MAP) kinase quantification, and H&E staining was performed on colonic tissues. Mucosa-associated microbiota composition was characterized by 16S ribosomal RNA sequencing. For the in vitro experiments, murine intestinal crypts and the human mucus-secreting HT29-methotrexate treated cell line were stimulated with MDX in the presence or absence of TUDCA or a p38 MAP kinase inhibitor.Diets enriched in MDX, but not propylene glycol or animal gelatin, exacerbated intestinal inflammation in both models. Analysis of the mechanisms underlying the detrimental effect of MDX showed up-regulation of inositol requiring protein 1β, a sensor of ER stress, in goblet cells, and a reduction of mucin-2 expression with no significant change in mucosa-associated microbiota. Stimulation of murine intestinal crypts and HT29-methotrexate treated cell line cells with MDX induced inositol requiring protein 1β via a p38 MAP kinase-dependent mechanism. Treatment of mice with TUDCA prevented mucin-2 depletion and attenuated colitis in MDX-fed mice.MDX increases ER stress in gut epithelial cells with the downstream effect of reducing mucus production and enhancing colitis susceptibility.

Federica Laudisi

Davide Di Fusco

Vincenzo Dinallo

Carmine Stolfi

Antonio Di Grazia

Irene Marafini

Alfredo Colantoni

Angela Ortenzi

Claudia Alteri

Francesca Guerrieri

Maria Mavilio

Francesca Ceccherini-Silberstein

Massimo Federici

Thomas Thornton MacDonald

Ivan Monteleone

Giovanni Monteleone

The Food Additive Maltodextrin Promotes Endoplasmic Reticulum Stress–Driven Mucus Depletion and Exacerbates Intestinal Inflammation

食品添加剂麦芽糊精促进内质网应激驱动的粘液耗竭并加剧肠道炎症

Hepatocytes Foxo1 controls the crosstalk between hepatocytes, macrophages, and HSC, via regulating TGF-β1 expression, to promote liver fibrosis.Hepatic FoxO1 may be a therapeutic target for prevention and treatment of liver fibrosis. Background & Aims:The O-class of the forkhead transcription factor FoxO1 is a crucial factor mediating insulin→PI3K→Akt signaling and governs diverse cellular processes.However, the role of hepatocyte FoxO1 in liver fibrosis has not been well established.In his study, we investigated the role of hepatocyte FoxO1 in liver fibrosis and uncovered the underlying mechanisms.Methods: Liver fibrosis was established by carbon tetrachloride (CCL4) administration and compared between liver-specific deletion of FoxO1 deletion (F1KO) and control (CNTR) mice.Using genetic and bioinformatic strategies in vitro and in vivo, the role of hepatic FoxO1 in liver fibrosis and associated mechanisms was established.Results: Increased FoxO1 expression and FoxO1 signaling activation were observed in CCL4induced fibrosis.Hepatic FoxO1 deletion largely attenuated CCL4-induced liver injury and fibrosis compared to CNTR mice.F1KO mice showed ameliorated CCL4-induced hepatic inflammation and decreased TGF-β1 mRNA and protein levels compared to those of CNTR mice.In primary hepatocytes, FoxO1 deficiency reduced TGF-β1 expression and secretion.Conditioned medium (CM) collected from WT hepatocytes treated with CCL4 activated human HSC cell line (LX-2), such effect was attenuated by FoxO1 deletion in primary hepatocytes or neutralization of TGF-β1 in the CM using TGF-β1 antibody.Hepatic FoxO1 overexpression in CNTR mice promoted CCL4-induced HSC activation; such effect was blocked in L-TGF-β1KO mice.

Quan Pan

Mingming Gao

DaMi Kim

Weiqi Ai

Wanbao Yang

Wen Jiang

Wesley Brashear

Yujiao Dai

Sha Li

Yuxiang Sun

Yajuan Qi

Shaodong Guo

Hepatocyte FoxO1 Deficiency Protects From Liver Fibrosis via Reducing Inflammation and TGF-β1-mediated HSC Activation

肝细胞FoxO1缺陷通过减少炎症和TGF-β1介导的HSC激活保护肝脏免受纤维化

Alcohol abuse is the most frequent precipitating factor of acute-on-chronic liver failure (ACLF). We aimed at developing an alcohol-induced ACLF model and dissecting its underlying molecular mechanisms.

Martí Ortega-Ribera

Yuan Zhuang

Mrigya Babuta

Veronika Brezani

Radhika S Joshi

Zsuzsanna Zsengeller

Prashanth Thevkar Nagesh

Yanbo Wang

Roderick Bronson

Gyongyi Szabo

A novel multi-organ male model of alcohol-induced acute-on-chronic liver failure reveals NET-mediated hepatocellular death which is prevented by RIPK3 inhibition

一种新型酒精性急性加慢性肝衰竭多器官雄性模型揭示了中性粒细胞胞外诱捕网介导的肝细胞死亡，该死亡可通过RIPK3抑制得以预防

Intestinal stem cells replenish the epithelium throughout life by continuously generating intestinal epithelial cell types, including absorptive enterocytes, and secretory goblet, endocrine, and Paneth cells. This process is orchestrated by a symphony of niche factors required to maintain intestinal stem cells and to direct their proliferation and differentiation. Among the various mature intestinal epithelial cell types, Paneth cells are unique in their location in the stem cell zone, directly adjacent to intestinal stem cells. Although Paneth cells were first described as an epithelial cell component of the innate immune system due to their expression of anti-microbial peptides, they have been proposed to be niche cells due to their close proximity to intestinal stem cells and expression of niche factors. However, function as a niche cell has been debated since mice lacking Paneth cells retain functional stem cells that continue to replenish the intestinal epithelium. In this review, we summarize the intestinal stem cell niche, including the Notch, Wnt, growth factor, mechanical, and metabolic niche, and discuss how Paneth cells might contribute to these various components. We also present a nuanced view of the Paneth cell as a niche cell. Although not required, Paneth cells enhance stem cell function, particularly during intestinal development and regeneration. Furthermore, we suggest that Paneth cell loss induces ISC remodeling to adjust their niche demands.

Michaela Quintero

Linda C Samuelson

Paneth Cells: Dispensable yet Irreplaceable for the Intestinal Stem Cell Niche

潘氏细胞：肠道干细胞龛中虽非必需却不可替代

Organs of the gastrointestinal tract contain tissue-resident immune cells that function during tissue development, homeostasis, and disease. However, most published human organoid model systems lack resident immune cells, thus limiting their potential as disease avatars. For example, human intestinal organoids (HIOs) derived from pluripotent stem cells contain epithelial and various mesenchymal cell types but lack immune cells. In this study, we aimed to develop an HIO model with functional tissue-resident macrophages.

Kentaro Tominaga

Daniel O Kechele

J Guillermo Sanchez

Simon Vales

Ingrid Jurickova

Lizza Roman

Akihiro Asai

Jacob R Enriquez

Heather A McCauley

Keishi Kishimoto

Kentaro Iwasawa

Akaljot Singh

Yuko Horio

Jorge O Múnera

Takanori Takebe

Aaron M Zorn

Michael A Helmrath

Lee A Denson

James M Wells

Deriving human intestinal organoids with functional tissue-resident macrophages all from pluripotent stem cells

从多能干细胞中衍生出具有功能性组织驻留巨噬细胞的人类肠道类器官

Noriyuki Nishiwaki

Kensuke Sugiura

Kensuke Suzuki

Alina L. Li

Constanza Tapia Contreras

Gizem Efe

Alice E. Shin

Dorsay Sadeghian

Jun Zhao

Anirban Maitra

Jason R. Pitarresi

Peter A. Sims

Rohit Chandwani

Anil K. Rustgi

PRRX1 has functional roles in pancreatic acinar to ductal metaplasia and carcinogenesis

PRRX1在胰腺腺泡向导管化生及癌变中具有功能性作用

Circadian disturbances result in adverse health effects, including gastrointestinal symptoms. We investigated which physiological pathways in jejunal mucosa were disrupted during chronic jetlag and prevented during time-restricted feeding (TRF). Enteroids from Bmal1+/+ and Bmal1-/- mice were used to replicate the processes that were affected by chronic jetlag and rescued by TRF.

Hui Leng

Theo Thijs

Louis Desmet

Guillaume Vanotti

Mona Farhadipour

Inge Depoortere

Time-restricted feeding reinforces gut rhythmicity by restoring rhythms in intestinal metabolism in a jetlag mouse model

限时进食通过恢复肠道代谢节律增强肠道节律性：以时差反应小鼠模型为研究对象

Abbreviation	Cell. Mol. Gastroenterol. Hepatol.
Journal Impact	6.96
Quartiles(Global)	GASTROENTEROLOGY & HEPATOLOGY(Q1)

ISSN	2352-345X
h-index	67

Publication Information	Publisher: Elsevier Inc.，Publishing cycle: ，Journal Type: journal，Open Access Journals: Yes
Basic data	Year of publication: 2015，Proportion of original research papers: 88.15%，Self Citation Rate:1.40%， Gold OA Rate: 75.23%
Journal Fees	$2500Details
Average review cycle	网友分享经验：19 Weeks

CMGH

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