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Advances in Liver Disease
State of the Journal: CMGH’s Progress, Prospects, and Impact Factor
Cellular and Molecular Gastroenterology and Hepatology (CMGH) was established to create a forum for high-quality, mechanistic studies of the gastrointestinal tract, liver, and pancreas. CMGH has now completed its third full year of publication and has developed a reputation as a rigorous and highly regarded platform for basic and translational research. CMGH has also become known for a prompt, fair, and transparent review process in which authors are treated with respect and have access to editors.Uncovering a Predictive Molecular Signature for the Onset of NASH-Related Fibrosis in a Translational NASH Mouse Model
The incidence of nonalcoholic steatohepatitis (NASH) is increasing. The pathophysiological mechanisms of NASH and the sequence of events leading to hepatic fibrosis are incompletely understood. The aim of this study was to gain insight into the dynamics of key molecular processes involved in NASH and to rank early markers for hepatic fibrosis.Lamin Deficiency in the Liver Sets the Stage for Nonalcoholic Steatohepatitis Development in Males
Nuclear lamins are type V intermediate filament proteins that play important roles in maintaining nuclear shape and in transcriptional regulation. Moreover, they serve as signaling scaffolds at the inner nuclear membrane.1 Nuclear lamins fall into 2 separate classes, A-type and B-type, which are encoded by distinct genes. Mutations in their genes lead to tissue-selective disease phenotypes, termed laminopathies, which can affect muscle, adipose tissue, bone, liver, or multiple tissues depending on the site of the mutation.Analysis of Hepatitis C Virus Particle Heterogeneity in Immunodeficient Human Liver Chimeric fah-/- Mice
Hepatitis C virus (HCV) is a leading cause of chronic liver diseases and the most common indication for liver transplantation in the United States. HCV particles in the blood of infected patients are characterized by heterogeneous buoyant densities, likely owing to HCV association with lipoproteins. However, clinical isolates are not infectious in vitro and the relative infectivity of the particles with respect to their buoyant density therefore cannot be determined, pointing to the need for better in vivo model systems.The Quest for Relevant Hepatocellular Carcinoma Biomarkers
Interest in the field of -omics within the past decade has led to further advancement in the understanding of numerous biochemical pathways as well as their dysregulation in pathology. The technologies allow characterization and quantification at various molecular levels (genes, transcription factors, proteins, and metabolites), enabling the study of key genetic and epigenetic pathways. Importantly, by phenotyping organisms at various molecular levels, -omics applications can be translated into molecular diagnostics and therapeutics in a clinical setting.Hepatocyte-Specific Deletion of Mouse Lamin A/C Leads to Male-Selective Steatohepatitis
Lamins are nuclear intermediate filament proteins that comprise the major components of the nuclear lamina. Mutations in LMNA, which encodes lamins A/C, cause laminopathies, including lipodystrophy, cardiomyopathy, and premature aging syndromes. However, the role of lamins in the liver is unknown, and it is unclear whether laminopathy-associated liver disease is caused by primary hepatocyte defects or systemic alterations.Epigenetics and Liver Fibrosis
Liver fibrosis arises because prolonged injury combined with excessive scar deposition within hepatic parenchyma arising from overactive wound healing response mediated by activated myofibroblasts. Fibrosis is the common end point for any type of chronic liver injury including alcoholic liver disease, nonalcoholic fatty liver disease, viral hepatitis, and cholestatic liver diseases. Although genetic influences are important, it is epigenetic mechanisms that have been shown to orchestrate many aspects of fibrogenesis in the liver.Specific Macronutrients Exert Unique Influences on the Adipose-Liver Axis to Promote Hepatic Steatosis in Mice
The factors that distinguish metabolically healthy obesity from metabolically unhealthy obesity are not well understood. Diet has been implicated as a determinant of the unhealthy obesity phenotype, but which aspects of the diet induce dysmetabolism are unknown. The goal of this study was to investigate whether specific macronutrients or macronutrient combinations provoke dysmetabolism in the context of isocaloric, high-energy diets.TRIF as a Novel Modulator of Liver Inflammation and Fibrosis
The central role of toll-like receptor 4 (TLR4) activation in nonalcoholic steatohepatitis (NASH) has been well-recognized, specifically its role in the activation of innate immune responses, hepatocyte apoptosis, and fibrosis. TLR4 could be activated by various signals; in the context of NASH dysregulation of gut microbial homeostasis, gut leakiness and consequent increase in bacteria-derived lipopolysaccharide (LPS) seem to play a major role. Activation of TLR4 involves adapter proteins including MyD88-adaptor-like and TRIF-related adaptor molecule (TRAM) recruiting Myd88 and TRIF, respectively, and ultimately leading to the activation of nuclear factor kappa B and/or interferon-regulatory factor 3 (IRF3).Endoplasmic Reticulum Stress Regulates Hepatic Bile Acid Metabolism in Mice
Cholestasis promotes endoplasmic reticulum (ER) stress in the liver, however, the effect of ER stress on hepatic bile acid metabolism is unknown. We aim to determine the effect of ER stress on hepatic bile acid synthesis and transport in mice.
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