<div><p><b>Background: </b>Tumor microenvironment(TME) reflects the intertwined crosstalk between cancer cells and tumor-infiltrating immune cells, affecting the efficiency of immunotherapy. Metabolic reprogramming, one of the major hallmarks of hepatocellular carcinoma(HCC), is unclear in the aspect of reshaping TME. In this study, we report the vital role of SLC1A5, the major glutamine transporter of tumor cells, in HCC progression and the formation of immunosuppressive TME.</p>

<div><p><b>Background: </b>The effects of sodium-glucose cotransporter-2 inhibitors (SGLT-2i) on liver and renal outcomes in patients with type 2 diabetes mellitus (T2DM) were demonstrated in recent trials. However, the magnitude of benefits associated with underlying metabolic dysfunction-associated steatotic liver disease (MASLD) remains unclear. We aimed to explore the risk of adverse liver and renal outcomes in patients with MASLD and T2DM taking SGLT-2i vs.

<div><p><strong><b>Background:</strong> </b><span class="NormalTextRun SCXW91602795 BCX0">Effective treatment for alcohol use disorder (AUD) is the cornerstone of preventing the development of alcohol-associated liver disease (ALD).

<div><p><b>Background:</p> </b><p>This open-label study assessed the safety and efficacy of vebicorvir (VBR)+AB-729+nucleos(t)ide reverse transcriptase inhibitor (NrtI) in virologically suppressed (VS) patients (pts) with hepatitis B e antigen (eAg) negative chronic hepatitis B infection (NCT04820686). VBR is a 1st-generation core inhibitor and AB-729 is a single trigger GalNAc-siRNA targeting all HBV RNA transcripts. Initial end of treatment (EOT) responses were previously described.

<div><p><b>Background:</p> </b><p>Hepatocellular carcinoma (HCC) is a major cause of mortality worldwide. Providing precision medicine to patients is a key unmet need. Preclinical models, when accurately reflecting human disease, offer an opportunity to understand varying therapeutic responses between different patient groups.</p>

<div><p><b>Background: </b>Iron-catalyzed formation of reactive oxygen species (ROS) increases after APAP overdose and triggers the mitochondrial permeability transition (MPT). Previous studies show that iron translocation from lysosomes into mitochondria by MCU in hepatocytes promotes the MPT after APAP. Kupffer cells are liver resident macrophages that are involved in uptake, processing, and export of iron. Here, our Aim was to investigate and compare the roles of MCU in hepatocytes and Kupffer cells in APAP hepatotoxicity. </p>

<div><p><b>Background: </b>Metabolic dysfunction-associated steatotic liver disease (MASLD) is a chronic, progressive disease with substantial morbidity and mortality and no approved treatments. Observational studies have linked aspirin use to reduced prevalence and progression of MASLD. However, the efficacy and safety of aspirin for reducing hepatic steatosis, inflammation, and fibrosis in patients with MASLD are unknown.</p>

<div><p><b>Background:</p> </b><p>Pragmatic endpoints, such as time-to-treatment discontinuation (TTD), defined as the duration from starting a medication to the date of treatment discontinuation or death, have been proposed as a potential efficacy endpoint for real-world practice. This study aims to analyze the frequency and severity of immune-related adverse events (irAEs) and TTD in patients with hepatocellular carcinoma (HCC) receiving Atezolizumab and Bevacizumab (A+B) treatment.</p>

<div><p><b>Background: </b>An unbiased ‘genome-first’ approach has the potential to expand the understanding of common coding and predicted loss-of-function (pLOF) variants associated with non-alcoholic fatty liver disease (NAFLD). Utilizing this approach, we aimed to uncover the functionality of pathogenic variants in <em>TM6SF2</em>.</p>

<div><p><b>Background: </b>Autoimmune hepatitis is a serious chronic liver disease with immune disorders, histological lesions and liver dysfunction, with a gradually increasing prevalence. Yet the cellular and molecular mechanisms of immune dysregulation in AIH are poorly understood.</p>