The fibrosis investigating navigator in diabetes (FIND): A tool to predict liver fibrosis risk in subjects with diabetes.

Background: Type 2 diabetes increases the risk of cirrhosis and liver cancer. Noninvasive and early assessment of liver fibrosis is essential. We aimed to develop a score to aid in the initial assessment of liver fibrosis in the diabetic population.

Activated hepatic stellate cell-derived Bmp-1 induces liver fibrosis via mediating hepatocyte epithelial-mesenchymal transition.

Liver fibrosis is a reparative response to injury that arises from various etiologies, characterized by activation of hepatic stellate cells (HSCs). Periostin, a secreted matricellular protein, has been reported to participate in tissue development and regeneration. However, its involvement in liver fibrosis remains unknown.

Hepatitis B virus X protein induces ALDH2 ubiquitin-dependent degradation to enhance alcoholic steatohepatitis.

Background: Excessive alcohol intake with hepatitis B virus (HBV) infection accelerates chronic liver disease progression and patients with HBV infection are more susceptible to alcohol-induced liver disease. Hepatitis B virus X protein (HBx) plays a crucial role in disease pathogenesis, while its specific role in alcoholic liver disease (ALD) progression has not yet been elucidated. Here, we studied the role of HBx on the development of ALD.

Diagnostic performance of elastography on liver fibrosis in antiviral treatment-naive chronic hepatitis B patients: a meta-analysis.

Background: This study aimed to assess the performance of transient elastography (TE), two-dimensional shear wave elastography (2D-SWE), and magnetic resonance elastography (MRE) for staging significant fibrosis and cirrhosis in untreated chronic hepatitis B (CHB) patients.

Methods: Pubmed, Embase, Web of Science, and Cochrane Library were searched for terms involving CHB, TE, 2D-SWE, and MRE. Other etiologies of chronic liver disease, previous treatment in patients, or articles not published in SCI journals were excluded.

ARRB1 suppresses the activation of hepatic macrophages via modulating endoplasmic reticulum stress in lipopolysaccharide-induced acute liver injury.

Acute liver injury (ALI) caused by multiple inflammatory responses is a monocyte-/macrophage-mediated liver injury that is associated with high morbidity and mortality. Liver macrophage activation is a vital event that triggers ALI. However, the mechanism of liver macrophage activation has not been fully elucidated.

A prognostic model for hepatocellular carcinoma patients based on signature ferroptosis-related genes.

Background: Considering the increase in the number of HCC patients, it is critical to predict the survival of patients. Although ferroptosis is closely related to HCC progression, predicting the survival of HCC patients through ferroptosis-related genes is challenging.

Methods: RNA-seq and clinical data of HCC in the TCGA database were analyzed to establish a prognostic model, and ICGC and GSE14520 data were used for validation.

Effectiveness and safety of endoscopic treatment for duodenal variceal bleeding: a systematic review.

Duodenal varix is a rare condition that involves massive bleeding, diagnostic difficulties, and a high rate of rebleeding and mortality. The purpose of this study was to systematically review endoscopic treatment for duodenal variceal bleeding to evaluate its effectiveness and safety. We searched PubMed, Embase, Web of Science, and the Cochrane Library up to 21 November 2019.

Ursolic acid reverses liver fibrosis by inhibiting interactive NOX4/ROS and RhoA/ROCK1 signalling pathways.

Liver fibrosis is the reversible deposition of extracellular matrix (ECM) and scar formation after liver damage by various stimuli. The interaction between NOX4/ROS and RhoA/ROCK1 in liver fibrosis is not yet clear. Ursolic acid (UA) is a traditional Chinese medicine with anti-fibrotic effects, but the molecular mechanism underlying these effects is still unclear.

Ursolic acid improves the bacterial community mapping of the intestinal tract in liver fibrosis mice.

Liver fibrosis often appears in chronic liver disease, with extracellular matrix (ECM) deposition as the main feature. Due to the presence of the liver-gut axis, the destruction of intestinal homeostasis is often accompanied by the development of liver fibrosis. The inconsistent ecological environment of different intestinal sites may lead to differences in the microbiota.

Assessing the Prognostic Performance of the Child-Pugh, Model for End-Stage Liver Disease, and Albumin-Bilirubin Scores in Patients with Decompensated Cirrhosis: A Large Asian Cohort from Gastroenterology Department.

Unlabelled: . Various methods, including the Child-Pugh score, the model for end-stage liver disease (MELD) score, the MELD combined with serum sodium concentration (MELD-Na) score, the integrated MELD (iMELD) score, and the albumin-bilirubin (ALBI) score, have been widely used for predicting the survival of decompensated cirrhosis (DeCi) patients. In this study, we defined and compared the prognostic value of these scores to predict mortality in DeCi patients.

Development of a prognostic scoring model for predicting the survival of elderly patients with hepatocellular carcinoma.

Background: The number of elderly hepatocellular carcinoma (HCC) patients is increasing, and precisely assessing of the prognosis of these patients is necessary. We developed a prognostic scoring model to predict survival in elderly HCC patients.

Methods: We extracted data from 4,076 patients ≥65 years old from the Surveillance, Epidemiology, and End Results (SEER) database and randomly divided them into training and validation groups.

Gut Microbial Dysbiosis Is Associated With Profibrotic Factors in Liver Fibrosis Mice.

Continuous development will evolve into end-stage liver disease. Profibrotic factors NOX4 and RhoA participate in the activation of HSC and accelerate the development of liver fibrosis. Abnormal intrahepatic metabolism during liver fibrosis interferes with intestinal homeostasis through the liver-gut axis.

Ursolic Acid Improves Intestinal Damage and Bacterial Dysbiosis in Liver Fibrosis Mice.

Liver fibrosis is a reversible process of extracellular matrix deposition or scar formation after liver injury. Intestinal damage and bacterial dysbiosis are important concomitant intestinal changes in liver fibrosis and may in turn accelerate the progression of liver fibrosis through the gut-liver axis. RhoA, an important factor in the regulation of the cytoskeleton, plays an important role in intestinal damage.

Protective Effect of Ursolic Acid on the Intestinal Mucosal Barrier in a Rat Model of Liver Fibrosis.

Oxidative stress mediated by nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX) plays an important role in intestinal mucosal barrier damage in various disease states. Recent evidence suggests that intestinal mucosal barrier damage and intestinal dysbiosis occur in mice with hepatic fibrosis induced by CCl4 or bile duct ligation. Another study showed that ursolic acid (UA) attenuates experimental colitis via its anti-inflammatory and antioxidant activities.

Systematic review with a meta-analysis: clinical effects of statins on the reduction of portal hypertension and variceal haemorrhage in cirrhotic patients.

Background: Statins may improve outcomes in patients with cirrhosis. We performed a systematic review and meta-analysis to evaluate the effect of statins on patients with cirrhosis and related complications, especially portal hypertension and variceal haemorrhage.

Methods: Studies were searched in the PubMed, Embase and Cochrane library databases up to February 2019.

Interaction Mechanisms Between the NOX4/ROS and RhoA/ROCK1 Signaling Pathways as New Anti- fibrosis Targets of Ursolic Acid in Hepatic Stellate Cells.

Background: Studies have shown that both NOX4 and RhoA play essential roles in fibrosis and that they regulate each other. In lung fibrosis, NOX4/ROS is located upstream of the RhoA/ROCK1 signaling pathway, and the two molecules are oppositely located in renal fibrosis. Currently, no reports have indicated whether the above mechanisms or other regulatory mechanisms exist in liver fibrosis.