ARRB1 downregulates acetaminophen-induced hepatoxicity through binding to p-eIF2α to inhibit ER stress signaling.

Acetaminophen (APAP) stands as the predominant contributor to drug-induced liver injury (DILI), and limited options are available. β-Arrestin1 (ARRB1) is involved in numerous liver diseases. However, the role of ARRB1 in APAP-induced liver injury remained uncertain.

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.

PTTG1 alleviates acute alcoholic liver injury by inhibiting endoplasmic reticulum stress-induced hepatocyte pyroptosis.

Background & Aims: Heavy drinking is a primary cause of alcoholic liver injury (ALI). Pituitary tumour transforming gene 1 (PTTG1) is involved in the occurrence and development of hepatocellular carcinoma (HCC), which is a well-known inflammation-related cancer with various aetiologies, including alcohol consumption. However, the role of PTTG1 in alcohol-induced liver injury and inflammation is not clear.

Integrated systemic analysis of FAM72A to identify its clinical relevance, biological function, and relationship to drug sensitivity in hepatocellular carcinoma.

Background: The family with sequence similarity 72 member A (FAM72A) protein has been identified as an effector of multiple pathological processes in many cancers. The value of FAM72A in HCC remains largely unknown.

Methods: Data from TCGA-LIHC, ICGC-LIRI-JP, IMvigor210, cBioPortal, GeneMANIA, and TIMER were processed and visualized to explore the association between FAM72A and the prognosis, stemness phenotype, mutational burden, immune cell infiltration, and drug sensitivity in HCC patients.

Effect of alcohol on clinical complications of hepatitis virus-induced liver cirrhosis: a consecutive ten-year study.

Background And Aims: Although coexisting alcohol-induced liver disease and hepatitis B or C virus-induced liver cirrhosis (ALD + HBV or ALD + HCV) has been the center of recent hepatology researches, numerous controversies still persist. This study aimed to showcase the influence of alcohol on the laboratory values and on the clinical outcomes of patients with hepatitis B and C virus-induced liver cirrhosis.

Methods: Patients diagnosed with liver cirrhosis (n = 22,287) from January 2010 to December 2019 were enrolled, and divided into five groups according to the etiology: alcohol-induced liver disease (ALD, 1652 cases), hepatitis B virus (HBV, 18,079 cases), hepatitis C virus (HCV, 682 cases), ALD + HBV (1594 cases) and ALD + HCV (280 cases).

FcGBP and VCAM-1 are ponderable biomarkers for differential diagnosis of alcoholic liver cirrhosis.

Background/ Aims: Early diagnosis of alcoholic liver cirrhosis (ALD) and coexisting ALD and hepatitis B virus-induced cirrhosis (ALD+HBV) is primordial for an optimal management of these conditions. However, the lack of specific noninvasive biomarkers coupled with the inaccuracy of self-reported alcohol consumption make the early diagnosis of these pathologies difficult. This study aimed to identify biomarkers to diagnose ALD and differentiate ALD+HBV from HBV.

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.

Phosphorylation of NF-κBp65 drives inflammation-mediated hepatocellular carcinogenesis and is a novel therapeutic target.

Background: Nuclear factor-κB (NF-κB) plays a vital role in hepatocellular carcinoma (HCC). β-arrestin1 (ARRB1) has been proved to enhance the activity of NF-κBp65, and our previous study indicated that ARRB1 promotes hepatocellular carcinogenesis and development of HCC. However, it remains unknown whether p65 is involved in hepatocellular carcinogenesis through the ARRB1-mediated pathway.

HBx induces hepatocellular carcinogenesis through ARRB1-mediated autophagy to drive the G/S cycle.

The hepatitis B virus X protein (HBx) is involved in the process of hepatocellular carcinoma via the activation of various oncogenes. Our previous study indicated that ARBB1 (arrestin beta 1) promotes hepatocellular carcinogenesis (HCC). However, the role of ARRB1 in HBx-related HCC remains unclear.

LINC00355:8 promotes cell proliferation and migration with invasion the MiR-6777-3p/Wnt10b axis in Hepatocellular Carcinoma.

Recent studies have reported that various long non-coding RNAs (lncRNAs) promote hepatocellular carcinoma (HCC) progression, and our previous study indicated that lncRNA LINC00355:8 is overexpressed in HCC. However, the role of LINC00355:8 in HCC is unclear. The primary aim of this study was to explore the biological role of LINC00355:8 in HCC.

β-Arrestin1 is involved in hepatocellular carcinoma metastasis via extracellular signal-regulated kinase-mediated epithelial-mesenchymal transition.

Background And Aim: Hepatocellular carcinoma (HCC) is a malignant disease worldwide. It is implicated in high cancer-related mortality rates in humans. β-Arrestin1 (ARRB1) has been demonstrated to be related to the development of several cancers, while the relationship between ARRB1 and metastasis in HCC is unknown.

Recurrent esophagogastric variceal bleeding due to portal vein thrombosis caused by protein S deficiency.

Esophagogastric variceal bleeding (EGVB) is common in patients with portal vein thrombosis (PVT). Hereditary deficiencies in natural anticoagulant proteins, such as protein S, might contribute to PVT. However, recurrent EGVB caused by PVT in patients with protein S deficiency is seldom reported.

Procedure-related complications in gastric variceal obturation with tissue glue.

Aim: To focus on procedure-related complications, evaluate their incidence, analyze the reasons and discuss the solutions.

Methods: Overall, 628 endoscopic gastric variceal obturation (EGVO) procedures (case-times) with NBC were performed in 519 patients in the Department of Endoscopy of the Third Affiliated Hospital of Sun Yat-Sen University from January 2011 to December 2016. The clinical data of patients and procedure-related complications of EGVO were retrospectively analyzed.

Diagnosis of eosinophilic gastroenteritis is easily missed.

Aim: To analyze the clinical characteristics of eosinophilic gastroenteritis (EGE) and to investigate the situations of missed diagnosis of EGE.

Methods: First, the clinical characteristics of 20 EGE patients who were treated at our hospital were retrospectively summarized. Second, 159 patients who underwent gastroscopy and 211 patients who underwent colonoscopy were enrolled.