Early identification of modifiable risk factors is essential for the prevention of NAFLD. We aimed to systematically explore the relationships between genetically predicted modifiable risk factors and nonalcoholic fatty liver disease (NAFLD).

Hepatitis B virus infection causes oxidative stress and alters mitochondria in experimental models. Our goal was to investigate if HBV might alter liver mitochondria also in human, and the resulting mitochondrial stress might account for the progression of fibrosis in chronic hepatitis B (CHB).

Chronic hepatitis D infection results in the most severe form of chronic viral hepatitis but currently lacks effective treatment options. Therapy with pegylated interferon alpha (PEG-IFNα) is recommended for finite treatment duration by major liver societies. Still, it is plagued by low rates of sustained virologic response (SVR) and frequent relapses even if SVR is achieved. Recently, a wave of new

The mammalian liver harbors heterogeneous cell types that communicate via local paracrine signaling. Recent studies have delineated the transcriptomic landscape of the liver in nonalcoholic steatohepatitis (NASH) that provides insights into liver cell heterogeneity, intercellular crosstalk, and disease-associated reprogramming. However, the nature of intrahepatic signaling and its role in NASH progression

The treatment of hepatocellular carcinoma (HCC) has been transformed by the use of immune checkpoint inhibitors. However, most patients with HCC do not benefit from treatment with immunotherapy. There is an urgent need to understand the mechanisms that underlie response or resistance to immunotherapy for patients with HCC. The use of syngeneic mouse models that closely recapitulate the heterogeneity

Chronic hepatitis B virus (HBV) infection is the leading cause of hepatocellular carcinoma (HCC) and is a serious health problem in China, East Asia, and North African countries. Effective treatment of HBV-related HCC is currently unavailable. This study evaluated the therapeutic potential of TIGIT blockade in HBV-related HCC.

Abstract

Abstract

Recent studies suggest that mitochondrial dysfunction promotes progression to non-alcoholic steatohepatitis (NASH) by aggravating the gut-liver status. However, the underlying mechanism remains unclear. Herein, we hypothesized that enhanced mitochondrial activity might reshape a specific microbiota signature that, when transferred to germ-free (GF) mice, could delay NASH progression.

Implantation of a transjugular intrahepatic portosystemic shunt (TIPS) improves survival in cirrhotic patients with refractory ascites and portal hypertensive bleeding. However, the indication for TIPS in older adult patients (≥70 years) is debated and a specific prediction model developed in this particular setting is lacking. The aim of this study was to develop and validate a multivariable model

Gain-of-function (GOF) mutations of CTNNB1 and loss-of-function (LOF) mutations of AXIN1 are recurrent genetic alterations in hepatocellular carcinoma (HCC). We aim to investigate the functional contribution of Hippo/YAP/TAZ in GOF CTNNB1 or LOF AXIN1 mutant HCCs.

The NADPH oxidase NOX4 plays a tumor suppressor function in hepatocellular carcinoma (HCC). Silencing NOX4 confers higher proliferative and migratory capacity to HCC cells and increases their in vivo tumorigenic potential in xenografts in mice. NOX4 gene deletions are frequent in HCC, correlating with higher tumor grade and worse recurrence-free and overall survival rates. However, despite of the accumulating

CONFLICT OF INTEREST Nothing to report.

Abstract

CONFLICT OF INTEREST Nothing to report.

Cell fate can be directly reprogrammed from accessible cell types (e.g., fibroblasts) into functional cell types by exposure to small molecule stimuli. However, no chemical reprogramming method has been reported to date that successfully generates functional hepatocyte-like cells that can repopulate liver tissue, casting doubt over the feasibility of chemical reprogramming approaches to obtain desirable

CONFLICT OF INTEREST Nothing to report.

Abstract

CONFLICT OF INTEREST Nothing to report.

CONFLICTS OF INTEREST Milan J. Sonneveld is on the speakers' bureau and received grants from Fujirebio. He received grants from Gilead. Robert J. de Knegt consults for and received grants from AbbVie. He is on the speakers’ bureau for Echosens. He received grants from Gilead and Janssen.

CONFLICT OF INTEREST M. Papatheodoridi: none; A.S. Lok: research grants from Bristol-Myers Squibb, Gilead, and TARGET; G.V. Papatheodoiridis: advisor/lecturer for Amgen, Gilead, GlaxoSmithKline, Ipsen, Janssen, Novo Nordisk, Roche, and Takeda and research grants from Gilead.

CONFLICT OF INTEREST Richard L. Ehman has intellectual property rights and a financial interest in magnetic resonance elastography. He serves as uncompensated CEO of Resoundant, Inc., a Mayo Clinic company. Meng Yen owns stock in Resoundant. She has intellectual property rights and a financial interest in magnetic resonance elastography. The Mayo Clinic has intellectual property rights and a financial

While the respiratory tract represents the primary target of severe acute respiratory distress syndrome coronavirus 2 (SARS-CoV-2) infection, it has become evident that COVID-19 is a multisystemic infectious disease. The hepatobiliary system could be affected during infection, ranging from slightly elevated liver enzymes to liver failure or secondary sclerosing cholangitis (SSC). Whether direct cytopathic

We thank Jiang et al.[1] for the interest in our study on progressive cholestasis and secondary sclerosing cholangitis (SSC) after coronavirus disease 2019 (COVID-19) in patients with chronic liver disease (CLD)[2] that has raised clinical awareness for long-term hepatobiliary complications of COVID-19. Importantly, patients with CLD, especially NAFLD/NASH, and those with severe courses of COVID-19

To the editor, Recently, Hartl et al. reported a study on liver-related complications after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection.[1] This single-center retrospective study includes 65 patients with NAFLD/NASH-predominant chronic liver disease (CLD). They described the pattern of progression of cholestatic liver injury following SARS-CoV-2 infection. Hartl et al. noted

CONFLICT OF INTEREST Nothing to report.