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Protease-induced excitation of dorsal root ganglion neurons in response to acute perturbation of the gut microbiota is associated with visceral and somatic hypersensitivity Cell. Mol. Gastroenterol. Hepatol. (IF 7.2) Pub Date : 2024-03-16 Corey C. Baker, Jessica L. Sessenwein, Hannah M. Wood, Yang Yu, Quentin Tsang, Taylor A. Alward, Nestor N. Jimenez Vargas, Amal Abu Omar, Abby McDonnel, Julia Segal, Calvin P. Sjaarda, Nigel W. Bunnett, Brian L. Schmidt, Alberto Caminero, Nadejda Boev, Courtney Bannerman, Nader Ghasemlou, Prameet M. Sheth, Stephen J. Vanner, David E. Reed, Alan E. Lomax
Abdominal pain is a major symptom of diseases that are associated with microbial dysbiosis, including irritable bowel syndrome and inflammatory bowel disease. Germ-free mice are more prone to abdominal pain than conventionally-housed mice, and reconstitution of the microbiota in germ-free mice reduces abdominal pain sensitivity. However, the mechanisms underlying microbial modulation of pain remain
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Replication efficiency of SARS-CoV-2 Omicron subvariants BA.2.75, BA.5, and XBB.1 in human mini-gut organoids Cell. Mol. Gastroenterol. Hepatol. (IF 7.2) Pub Date : 2024-03-15 Kei Miyakawa, Masakazu Machida, Tomoyuki Kawasaki, Masatoshi Kakizaki, Yayoi Kimura, Masaya Sugiyama, Hideki Hasegawa, Akihiro Umezawa, Hidenori Akutsu, Akihide Ryo
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Enteric nervous system striped patterning and disease: unexplored pathophysiology Cell. Mol. Gastroenterol. Hepatol. (IF 7.2) Pub Date : 2024-03-11 Lori B. Dershowitz, Julia A. Kaltschmidt
The enteric nervous system (ENS) controls gastrointestinal (GI) motility, and defects in ENS development underlie pediatric GI motility disorders. In disorders such as Hirschsprung’s disease (HSCR), pediatric intestinal pseudo-obstruction (PIPO), and intestinal neuronal dysplasia type B (INDB), ENS structure is altered with noted decreased neuronal density in HSCR and reports of increased neuronal
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Endothelial Slc35a1 deficiency causes loss of LSEC identity and exacerbates neonatal lipid deposition in the liver in mice Cell. Mol. Gastroenterol. Hepatol. (IF 7.2) Pub Date : 2024-03-11 Bin Zuo, Fei Yang, Lulu Huang, Jingjing Han, Tianyi Li, Zhenni Ma, Lijuan Cao, Yun Li, Xia Bai, Miao Jiang, Yang He, Lijun Xia
The functional maturation of the liver largely occurs after birth. In the early stages of life, the liver of a newborn encounters enormous high-fat metabolic stress caused by the consumption of breast milk. It is unclear how the maturing liver adapts to high lipid metabolism. Liver sinusoidal endothelial cells (LSECs) play a fundamental role in establishing liver vasculature and are decorated with
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Location Matters: Mitochondrial Arginase 2 as a Treatment for Metabolic Disease? Cell. Mol. Gastroenterol. Hepatol. (IF 7.2) Pub Date : 2024-03-10 Megan Stefkovich, Paul M. Titchenell
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Platelets in Alcohol-associated Liver Disease - Interaction with Neutrophils Cell. Mol. Gastroenterol. Hepatol. (IF 7.2) Pub Date : 2024-03-08 Juan Wang, Xianda Wang, Haodong Peng, Zijian Dong, Suthat Liangpunsakul, Li Zuo, Hua Wang
Alcohol-associated liver disease (ALD) is a major contributor to liver-related mortality globally. A growing body of evidence underscores the pivotal role of platelets throughout the spectrum of liver injury and recovery, offering unique insights into liver homeostasis and pathobiology. Alcoholic-associated steatohepatitis is characterized by the infiltration of hepatic neutrophils. Recent studies
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Autophagy contributes to homeostasis in esophageal epithelium where high autophagic vesicle level marks basal cells with limited proliferation and enhanced self-renewal potential Cell. Mol. Gastroenterol. Hepatol. (IF 7.2) Pub Date : 2024-03-05 Alena Klochkova, Adam L. Karami, Annie D. Fuller, Louis R. Parham, Surali R. Panchani, Shruthi Natarajan, Jazmyne L. Jackson, Anbin Mu, Yinfei Tan, Kathy Q. Cai, Andres J. Klein-Szanto, Amanda B. Muir, Marie-Pier Tétreault, Xavier Graña, Kathryn E. Hamilton, Kelly A. Whelan
Autophagy plays roles in esophageal pathologies both benign and malignant. Here, we aim to define the role of autophagy in esophageal epithelial homeostasis. We generated tamoxifen-inducible, squamous epithelial-specific (autophagy related 7) conditional knockout mice to evaluate effects on esophageal homeostasis and response to the carcinogen 4-nitroquinoline 1-oxide (4NQO) using histological and
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Colitis-induced small intestinal hypomotility is dependent on enteroendocrine cell loss in mice Cell. Mol. Gastroenterol. Hepatol. (IF 7.2) Pub Date : 2024-03-02 Zachariah Raouf, Steve N. Steinway, Daniel Scheese, Carla M. Lopez, Johannes W. Duess, Koichi Tsuboi, Maame Sampah, Daphne Klerk, Mahmoud El Baassiri, Hannah Moore, Cody Tragesser, Thomas Prindle, Sanxia Wang, Menghan Wang, Hee-Seong Jang, William B. Fulton, Chhinder P. Sodhi, David J. Hackam
The abdominal discomfort experienced by patients with colitis may be attributable in part to the presence of small intestinal dysmotility, yet mechanisms linking colonic inflammation with small bowel motility remain largely unexplored. We hypothesize that colitis results in small intestinal hypomotility due to a loss of enteroendocrine cells (EECs) within the small intestine that can be rescued using
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Role of ICAM-1 in the Adhesion of T Cells to Enteric Glia: Perspectives in the Formation of Plexitis in Crohn’s Disease Cell. Mol. Gastroenterol. Hepatol. (IF 7.2) Pub Date : 2024-02-29 Julie Pabois, Tony Durand, Catherine Le Berre, Rhiannon T. Filippone, Théo Noël, Emilie Durieu, Céline Bossard, Sarah Bruneau, Malvyne Rolli-Derkinderen, Kulmira Nurgali, Michel Neunlist, Arnaud Bourreille, Isabelle Neveu, Philippe Naveilhan
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. T cells close to myenteric neural cells were retrospectively quantified in ileocolonic resections from 9 control subjects
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Trailblazing TRAIL Therapy: Illuminating Pathways for Cholangiocarcinoma Treatment Cell. Mol. Gastroenterol. Hepatol. (IF 7.2) Pub Date : 2024-02-29 Sungjin Ko
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Fatty Acid Oxidation Promotes Apoptotic Resistance and Proinflammatory Phenotype of CD4+ Tissue-resident Memory T cells in Crohn’s Disease Cell. Mol. Gastroenterol. Hepatol. (IF 7.2) Pub Date : 2024-02-28 Guanzhan Liang, Junfeng Huang, Jing Chen, Xiaofeng Wen, Ruibing Li, Hanlin Xie, Zongjin Zhang, Zexian Chen, Yongle Chen, Zhenyu Xian, Xiaowen He, Jia Ke, Lei Lian, Ping Lan, Xianrui Wu, Tuo Hu
As the most abundant memory T cells and major source of tumor necrosis factor α in the intestinal mucosa of Crohn’s disease (CD) patients, CD4 tissue-resident memory T (T) cells play a critical role in CD pathogenesis. We investigated the role of metabolic reprogramming in the regulation of proinflammatory and apoptosis-resistant phenotype for CD4 T cells. CD4 T cells were collected from intestinal
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Fibroblast Growth Factor 19 Alters Bile Acids to Induce Dysbiosis in Mice With Alcohol-Induced Liver Disease Cell. Mol. Gastroenterol. Hepatol. (IF 7.2) Pub Date : 2024-02-28 Jessica M. Ferrell, Matthew Dilts, Sabita Pokhrel, Zachary Stahl, Shannon Boehme, Xinwen Wang, John Y.L. Chiang
Excessive alcohol consumption can lead to alcohol-associated liver disease, a spectrum of conditions ranging from steatosis to fibrosis and cirrhosis. Bile acids regulate metabolic pathways by binding to cellular and nuclear receptors, and they also interact with the gut microbiome to control microbial overgrowth. Fibroblast growth factor 19 (FGF-19) is an ileum-derived hormone induced and released
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A Nutraceutical Mechanistic Model Receives a Gut Check Cell. Mol. Gastroenterol. Hepatol. (IF 7.2) Pub Date : 2024-02-24 Nicholas J. Hand
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Actinomyces odontolyticus: From Carries to Colorectal Cancer Cell. Mol. Gastroenterol. Hepatol. (IF 7.2) Pub Date : 2024-02-22 Keith A. Breau
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Sex Matters: From Bile Acid Metabolism to Liver Cancer Cell. Mol. Gastroenterol. Hepatol. (IF 7.2) Pub Date : 2024-02-19 Sachin Kumar Singh Chauhan, Bernd Heinrich
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Cover - Blocking BRP39 Alters the Course of Liver Inflammation Cell. Mol. Gastroenterol. Hepatol. (IF 7.2) Pub Date : 2024-02-16
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Downregulation of V-ATPase V0 sector induces microvillus atrophy independently of apical trafficking in the mammalian intestine. Cell. Mol. Gastroenterol. Hepatol. (IF 7.2) Pub Date : 2024-02-16 Aurélien Bidaud-Meynard, Anne Bourdais, Ophélie Nicolle, Maela Duclos, Jad Saleh, Frank Ruemmele, Henner F. Farin, Delphine Delacour, Despina Moshous, Grégoire Michaux
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The Fibroblast Landscape in Stomach Carcinogenesis Cell. Mol. Gastroenterol. Hepatol. (IF 7.2) Pub Date : 2024-02-09 Ela W. Contreras-Panta, Eunyoung Choi, James R. Goldenring
Numerous recent studies using single cell RNA sequencing and spatial transcriptomics have shown the vast cell heterogeneity, including epithelial, immune, and stromal cells, present in the normal human stomach and at different stages of gastric carcinogenesis. Fibroblasts within the metaplastic and dysplastic mucosal stroma represent key contributors to the carcinogenic microenvironment in the stomach
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Lysyl Oxidase Regulates Epithelial Differentiation and Barrier Integrity in Eosinophilic Esophagitis Cell. Mol. Gastroenterol. Hepatol. (IF 7.2) Pub Date : 2024-02-09 Masaru Sasaki, Takeo Hara, Joshua X. Wang, Yusen Zhou, Kanak V. Kennedy, Nicole N. Umeweni, Maiya A. Alston, Zachary C. Spergel, Satoshi Ishikawa, Ryugo Teranishi, Ritsu Nakagawa, Emily A. Mcmillan, Kelly A. Whelan, Tatiana A. Karakasheva, Kathryn E. Hamilton, Melanie A. Ruffner, Amanda B. Muir
Epithelial disruption in eosinophilic esophagitis (EoE) encompasses both impaired differentiation and diminished barrier integrity. We have shown that lysyl oxidase (LOX), a collagen cross-linking enzyme, is upregulated in the esophageal epithelium in EoE. However, the functional roles of LOX in the esophageal epithelium remains unknown. We investigated roles for LOX in the human esophageal epithelium
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Myeloid Deletion of Cdc42 Protects Liver From Hepatic Ischemia-Reperfusion Injury Via Inhibiting Macrophage-Mediated Inflammation in Mice Cell. Mol. Gastroenterol. Hepatol. (IF 7.2) Pub Date : 2024-02-09 Jing He, Meng-Yu Tang, Li-Xin Liu, Chen-Xian Kong, Wen Chen, Lu Wang, Shao-Bin Zhi, Hong-Wei Sun, Yu-Chun Huang, Guo-Yu Chen, Hong-Bo Xin, Ke-Yu Deng
Hepatic ischemia-reperfusion injury (HIRI) often occurs in liver surgery such as partial hepatectomy and liver transplantation, in which myeloid macrophage-mediated inflammation plays a critical role. Cell division cycle 42 (Cdc42) regulates cell migration, cytoskeleton rearrangement and cell polarity. In this study, we aim to explore the role of myeloid Cdc42 in HIRI. Mouse HIRI models were established
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Stromal Niche Signals That Orchestrate Intestinal Regeneration Cell. Mol. Gastroenterol. Hepatol. (IF 7.2) Pub Date : 2024-02-09 Helen E. Abud, Shanika L. Amarasinghe, Diana Micati, Thierry Jardé
Stromal cell populations have a central role in providing signals that support the maintenance, differentiation, and function of the intestinal epithelium. The behavior and fate of epithelial cells is directed by the spatial organization of stromal cells that either sustain stem and progenitor cell identity or drive differentiation. A combination of single-cell analyses, mouse models, and organoid
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Telocytes in the Luminal GI Tract Cell. Mol. Gastroenterol. Hepatol. (IF 7.2) Pub Date : 2024-02-09 Michal Shoshkes-Carmel
Telocytes are unique mesenchymal cells characterized by multiple remarkably long cytoplasmic extensions that extend hundreds of micron away from the cell body. Through these extensions, telocytes establish a 3-dimensional network by connecting with other telocytes and various cell types within the tissue. In the intestine, telocytes have emerged as an essential component of the stem cell niche, providing
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Advances in Brain-Gut-Microbiome Interactions: A Comprehensive Update on Signaling Mechanisms, Disorders, and Therapeutic Implications Cell. Mol. Gastroenterol. Hepatol. (IF 7.2) Pub Date : 2024-02-08 Tien S. Dong, Emeran Mayer
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Multiple genes core to ERAD, macro-autophagy and lysosomal degradation pathways participate in the proteostasis response in α1-antitrypsin deficiency Cell. Mol. Gastroenterol. Hepatol. (IF 7.2) Pub Date : 2024-02-07 Jie Li, Francesca Moretti, Tunda Hidvegi, Sanja Sviben, James AJ. Fitzpatrick, Hemalatha Sundaramoorthi, Stephen C. Pak, Gary A. Silverman, Britta Knapp, Ireos Filipuzzi, John Alford, John Reece-Hoyes, Florian Nigsch, Leon O. Murphy, Beat Nyfeler, David H. Perlmutter
In the classical form of α1-antitrypsin deficiency (ATD), the misfolded α1-antitrypsin Z (ATZ) variant accumulates in the endoplasmic reticulum (ER) of liver cells. A gain-of-function proteotoxic mechanism is responsible for chronic liver disease in a sub-group of homozygotes. Proteostatic response pathways, including conventional ERAD and autophagy, have been proposed as the mechanisms that allow
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The Proteomic Signature of Tissue Remodeling in Chronic Intestinal Inflammation Cell. Mol. Gastroenterol. Hepatol. (IF 7.2) Pub Date : 2024-02-06 Markus F. Neurath
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Promises and Limitations of Current Models for Understanding Barrett’s Esophagus and Esophageal Adenocarcinoma Cell. Mol. Gastroenterol. Hepatol. (IF 7.2) Pub Date : 2024-02-06 Omar Martinez-Uribe, Thomas C. Becker, Katherine S. Garman
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). This expert review was written based on a thorough review of the literature combined with expert interpretation of the state of
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MCPIP1 Inhibits Hepatic Stellate Cell Activation in Autocrine and Paracrine Manners, Preventing Liver Fibrosis Cell. Mol. Gastroenterol. Hepatol. (IF 7.2) Pub Date : 2024-02-03 Natalia Pydyn, Anna Ferenc, Katarzyna Trzos, Ewelina Pospiech, Mateusz Wilamowski, Olga Mucha, Piotr Major, Justyna Kadluczka, Pedro M. Rodrigues, Jesus M. Banales, Jose M. Herranz, Matias A. Avila, Tomasz Hutsch, Piotr Malczak, Dorota Radkowiak, Andrzej Budzynski, Jolanta Jura, Jerzy Kotlinowski
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Rethinking the Roles of Cancer-Associated Fibroblasts in Pancreatic Cancer Cell. Mol. Gastroenterol. Hepatol. (IF 7.2) Pub Date : 2024-02-03 Ralph Francescone, Howard C. Crawford, Debora Barbosa Vendramini-Costa
Bearing a dismal 5-year survival rate, pancreatic ductal adenocarcinoma (PDAC) is a challenging disease that features a unique fibroinflammatory tumor microenvironment. As major components of the PDAC tumor microenvironment, cancer-associated fibroblasts are still poorly understood and their contribution to the several hallmarks of PDAC, such as resistance to therapies, immunosuppression, and high
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Epithelial-Fibroblast Crosstalk in Eosinophilic Esophagitis Cell. Mol. Gastroenterol. Hepatol. (IF 7.2) Pub Date : 2024-02-03 Amanda B. Muir, Tatiana A. Karakasheva, Kelly A. Whelan
Eosinophilic esophagitis (EoE) is an emerging form of food allergy that exerts a significant clinical and financial burden worldwide. EoE is clinically characterized by eosinophil-rich inflammatory infiltrates in esophageal mucosa and esophageal dysfunction. Remodeling events in esophageal epithelium and lamina propria also frequently occur in patients with EoE. Because subepithelial fibrosis is associated
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A Murine Model of Maternal Micronutrient Deficiencies and Gut Inflammatory Host-microbe Interactions in the Offspring Cell. Mol. Gastroenterol. Hepatol. (IF 7.2) Pub Date : 2024-02-02 Ravi Holani, Paula T. Littlejohn, Karlie Edwards, Charisse Petersen, Kyung-Mee Moon, Richard G. Stacey, Tahereh Bozorgmehr, Zachary J. Gerbec, Antonio Serapio-Palacios, Zakhar Krekhno, Katherine Donald, Leonard J. Foster, Stuart E. Turvey, B. Brett Finlay
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Fibroblasts in Orchestrating Colorectal Tumorigenesis and Progression Cell. Mol. Gastroenterol. Hepatol. (IF 7.2) Pub Date : 2024-02-02 Subinuer Abudukelimu, Noel F.C.C. de Miranda, Lukas J.A.C. Hawinkels
Cancer-associated fibroblasts (CAFs) are an abundant component of the tumor microenvironment and have been shown to possess critical functions in tumor progression. Although their roles predominantly have been described as tumor-promoting, more recent findings have identified subsets of CAFs with tumor-restraining functions. Accumulating evidence underscores large heterogeneity in fibroblast subsets
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Uncovering the Relationship Between Genes and Phenotypes Beyond the Gut in Microvillus Inclusion Disease Cell. Mol. Gastroenterol. Hepatol. (IF 7.2) Pub Date : 2024-02-02 Mingyue Sun, Olena Pylypenko, Zhe Zhou, Mingqian Xu, Qinghong Li, Anne Houdusse, Sven C.D. van IJzendoorn
Microvillus inclusion disease (MVID) is a rare condition that is present from birth and affects the digestive system. People with MVID experience severe diarrhea that is difficult to control, cannot absorb dietary nutrients, and struggle to grow and thrive. In addition, diverse clinical manifestations, some of which are life-threatening, have been reported in cases of MVID. MVID can be caused by variants
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Gut Bacteria-derived Membrane Vesicles Induce Colonic Dysplasia by Inducing DNA Damage in Colon Epithelial Cells Cell. Mol. Gastroenterol. Hepatol. (IF 7.2) Pub Date : 2024-02-01 Yu Miyakawa, Motoyuki Otsuka, Chikako Shibata, Takahiro Seimiya, Keisuke Yamamoto, Rei Ishibashi, Takahiro Kishikawa, Eri Tanaka, Takayuki Isagawa, Norihiko Takeda, Noriaki Kamio, Kenichi Imai, Mitsuhiro Fujishiro
Colorectal cancer (CRC) is the third most common cancer in the world. Gut microbiota has recently been implicated in the development of CRC. is one of the most abundant bacteria in the gut of patients with very early stages of CRC. is an anaerobic bacterium existing principally in the oral cavity, similar to which is known as a colon carcinogenic bacterium. Here we newly determined the biological functions
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CDKN2A-p16 deletion and activated KRASG12D drive Barrett’s-like gland hyperplasia-metaplasia and synergize in the development of dysplasia pre-cancer lesions Cell. Mol. Gastroenterol. Hepatol. (IF 7.2) Pub Date : 2024-01-29 Jing Sun, Jorge L. Sepulveda, Elena V. Komissarova, Caitlin Hills, Tyler D. Seckar, Narine M. LeFevre, Hayk Simonyan, Colin Young, Gloria Su, Armando Del Portillo, Timothy C. Wang, Antonia R. Sepulveda
Background & Aims Barrett’s esophagus (BE) is the precursor of esophageal dysplasia and adenocarcinoma (EAC). CDKN2A-p16 deletions were reported in 34-74% of BE patients who progressed to dysplasia and EAC, suggesting that p16 loss may drive neoplastic progression. KRAS activation frequently occurs in EAC and pre-cancer lesions. LGR5+ stem cells in the squamocolumnar-junction (SCJ) of mouse stomach
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The Interleukin 33–T Helper 2 Cell Axis Promotes Human Liver Fibrosis Cell. Mol. Gastroenterol. Hepatol. (IF 7.2) Pub Date : 2024-01-27 Isabella Lurje, Frank Tacke
Abstract not available
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A Structure-function Analysis of Hepatocyte Arginase 2 Reveals Mitochondrial Ureahydrolysis as a Determinant of Glucose Oxidation Cell. Mol. Gastroenterol. Hepatol. (IF 7.2) Pub Date : 2024-01-25 Yiming Zhang, Jiameng Sun, Henry D. Wasserman, Joshua A. Adams, Cassandra B. Higgins, Shannon C. Kelly, Louise Lantier, Brian J. DeBosch
Restoring hepatic and peripheral insulin sensitivity is critical to prevent or reverse metabolic syndrome and type 2 diabetes. Glucose homeostasis comprises in part the complex regulation of hepatic glucose production and insulin-mediated glucose uptake and oxidation in peripheral tissues. We previously identified hepatocyte arginase 2 (Arg2) as an inducible ureahydrolase that improves glucose homeostasis
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Optogenetic activation of cholinergic enteric neurons reduces inflammation in experimental colitis Cell. Mol. Gastroenterol. Hepatol. (IF 7.2) Pub Date : 2024-01-24 Ahmed A. Rahman, Rhian Stavely, Weikang Pan, Leah Ott, Kensuke Ohishi, Takahiro Ohkura, Christopher Han, Ryo Hotta, Allan M. Goldstein
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Sex Dimorphic Effects of Bile Acid Metabolism in Liver Cancer in Mice Cell. Mol. Gastroenterol. Hepatol. (IF 7.2) Pub Date : 2024-01-21 Rachel M. Golonka, Beng San Yeoh, Piu Saha, Yuan Tian, John Y.L. Chiang, Andrew D. Patterson, Andrew T. Gewirtz, Bina Joe, Matam Vijay-Kumar
Hepatocellular carcinoma (HCC) is a male-dominant disease, but targeted sex hormone therapies have not been successful. Bile acids are a potential liver carcinogen and are biomolecules with hormone-like effects. A few studies highlight their potential sex dimorphism in physiology and disease. We hypothesized that bile acids could be a potential molecular signature that explains sex disparity in HCC
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Oral Supplementation of Phosphatidylcholine Attenuates the Onset of a Diet-Induced Metabolic Dysfunction–Associated Steatohepatitis in Female C57BL/6J Mice Cell. Mol. Gastroenterol. Hepatol. (IF 7.2) Pub Date : 2024-01-21 Victor Sánchez, Anja Baumann, Annette Brandt, Maximilian F. Wodak, Raphaela Staltner, Ina Bergheim
Changes in phosphatidylcholine levels in the liver have been associated with the development of metabolic dysfunction–associated steatotic liver disease. Here, the effects of supplementing phosphatidylcholine on the development of early signs of metabolic dysfunction–associated steatohepatitis were assessed. Male and female C57BL/6J mice were fed a liquid control or a fructose-, fat-, and/or cholesterol-rich
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Cancer-Associated Fibroblasts in Esophageal Cancer Cell. Mol. Gastroenterol. Hepatol. (IF 7.2) Pub Date : 2024-01-19 Karen J. Dunbar, Kwok K. Wong, Anil K. Rustgi
Cancer-associated fibroblasts (CAFs), a heterogenous population, can promote cancer cell proliferation, migration, invasion, immunosuppression, and therapeutic resistance in solid tumors. These effects are mediated through secretion of cytokines and growth factors, remodeling of the extracellular matrix, and providing metabolic support for cancer cells. The presence of CAFs in esophageal carcinoma
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Stromal Cell Regulation of Intestinal Inflammatory Fibrosis Cell. Mol. Gastroenterol. Hepatol. (IF 7.2) Pub Date : 2024-01-19 Wenjing Yang, Tianming Yu, Yingzi Cong
Intestinal inflammatory fibrosis is a severe consequence of inflammatory bowel diseases (IBDs). There is currently no cure for the treatment of intestinal fibrosis in IBD. Although inflammation is necessary for triggering fibrosis, the anti-inflammatory agents used to treat IBD are ineffective in preventing the progression of intestinal fibrosis and stricture formation once initiated, suggesting that
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Cover - Interferon Epsilon (sub heading) Guardian of the Gut Cell. Mol. Gastroenterol. Hepatol. (IF 7.2) Pub Date : 2024-01-17
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Noncanonical TRAIL Signaling Promotes Myeloid-Derived Suppressor Cell Abundance and Tumor Growth in Cholangiocarcinoma Cell. Mol. Gastroenterol. Hepatol. (IF 7.2) Pub Date : 2024-01-14 Emilien J. Loeuillard, Binbin Li, Hannah E. Stumpf, Jingchun Yang, Jessica R. Willhite, Jennifer L. Tomlinson, Fred Rakhshan Rohakhtar, Vernadette A. Simon, Rondell P. Graham, Rory L. Smoot, Haidong Dong, Sumera I. Ilyas
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Cellular Interactions and Crosstalk Facilitating Biliary Fibrosis in Cholestasis Cell. Mol. Gastroenterol. Hepatol. (IF 7.2) Pub Date : 2024-01-10 Ludovica Ceci, Eugenio Gaudio, Lindsey Kennedy
Biliary fibrosis is seen in cholangiopathies, including primary biliary cholangitis (PBC) and primary sclerosing cholangitis (PSC). In PBC and PSC, biliary fibrosis is associated with worse outcomes and histologic scores. Within the liver, both hepatic stellate cells (HSCs) and portal fibroblasts (PFs) contribute to biliary fibrosis, but their roles can differ. PFs reside near the bile ducts and may
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“The Good, the Bad, and the Ugly” – About Diverse Phenotypes of Hepatic Stellate Cells in the Liver Cell. Mol. Gastroenterol. Hepatol. (IF 7.2) Pub Date : 2024-01-10 Alexandra Bogomolova, Asha Balakrishnan, Michael Ott, Amar Deep Sharma
Hepatic stellate cells (HSCs) and their activated derivatives, often referred to as myofibroblasts (MFs), play a key role in progression of chronic liver injuries leading to fibrosis, cirrhosis, and hepatocellular carcinoma. Until recently, MFs were considered a homogenous cell type majorly due to lack of techniques that allow complex molecular studies at a single-cell resolution. Recent technical
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Extracellular Matrix Orchestration of Tissue Remodeling in the Chronically Inflamed Mouse Colon Cell. Mol. Gastroenterol. Hepatol. (IF 7.2) Pub Date : 2024-01-09 Elisa B. Moutin, Joanna Bons, Giada Giavara, Filipe Lourenco, Deng Pan, Jordan B. Burton, Samah Shah, Mathilde Colombé, Philippe Gascard, Thea Tlsty, Birgit Schilling, Douglas J. Winton
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The Protease Domain in HEV pORF1 Mediates the Replicase’s Localization to Multivesicular Bodies and Its Exosomal Release Cell. Mol. Gastroenterol. Hepatol. (IF 7.2) Pub Date : 2024-01-06 Mirco Glitscher, Inga Mareike Spannaus, Fabiane Behr, Robin Oliver Murra, Kathrin Woytinek, Daniela Bender, Eberhard Hildt
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New Insights About Epigenetic Mechanisms That Influence Risk of Transgenerational Fatty Liver Disease Cell. Mol. Gastroenterol. Hepatol. (IF 7.2) Pub Date : 2023-12-30 David A. Rudnick
Abstract not available
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Germline Genetic Associations for Hepatobiliary Cancers Cell. Mol. Gastroenterol. Hepatol. (IF 7.2) Pub Date : 2023-12-30 Perapa Chotiprasidhi, Angela Karina Sato-Espinoza, Kirk J. Wangensteen
Hepatobiliary cancers (HBCs) include hepatocellular carcinoma, cholangiocarcinoma, and gallbladder carcinoma, which originate from the liver, bile ducts, and gallbladder, respectively. They are responsible for a substantial burden of cancer-related deaths worldwide. Despite knowledge of risk factors and advancements in therapeutics and surgical interventions, the prognosis for most patients with HBC
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Th2 Cell Activation in Chronic Liver Disease Is Driven by Local IL33 and Contributes to IL13-Dependent Fibrogenesis Cell. Mol. Gastroenterol. Hepatol. (IF 7.2) Pub Date : 2023-12-28 Johanna Reißing, Marie Berres, Pavel Strnad, Alexander Wree, Maria Eugenia Inzaugarat, Christian Trautwein, Tony Bruns, Henning Wolfgang Zimmermann
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Modulation of Hepatocyte Nuclear Factor 4 Alpha (HNF4α): A Critical Mechanism of Disease Progression in Liver Cirrhosis Cell. Mol. Gastroenterol. Hepatol. (IF 7.2) Pub Date : 2023-12-26 Udayan Apte
Abstract not available
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The Interplay of TGF-β1 and Cholesterol Orchestrating Hepatocyte Cell Fate, EMT, and Signals for HSC Activation Cell. Mol. Gastroenterol. Hepatol. (IF 7.2) Pub Date : 2023-12-27 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
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
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Altered B-Cell Expansion and Maturation in Draining Mesenteric Lymph Nodes of Inflamed Gut in Crohn’s Disease Cell. Mol. Gastroenterol. Hepatol. (IF 7.2) Pub Date : 2023-12-24 Sonja Kappel-Latif, Prasanti Kotagiri, Lukas Schlager, Gabor Schuld, Natalie Walterskirchen, Vanessa Schimek, Gavin Sewell, Carina Binder, Johanna Jobst, Supriya Murthy, Barbara Messner, Stefanie Dabsch, Arthur Kaser, Paul A. Lyons, Michael Bergmann, Anton Stift, Rudolf Oehler, Lukas W. Unger
Abstract not available
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The Recurrent Liver MAN2A1-FER Oncoprotein Lacks Kinase Activity: Implications for the Use of Tyrosine Kinase Inhibitors Cell. Mol. Gastroenterol. Hepatol. (IF 7.2) Pub Date : 2023-12-22 Mathieu Desaunay, Edwige Voisset, Sebastien Letard, Philippe Roche, Paulo De Sepulveda
Abstract not available