<div><p><b>Background:</p> </b><p>Metabolic dysfunction-associated steatohepatitis (MASH) patients who have developed stage F4 fibrosis (cirrhosis) are at risk of hepatic decompensation, hepatocellular carcinoma, liver transplant, cardiovascular events, liver and all-cause mortality. There are currently no approved therapies for non-cirrhotic or cirrhotic MASH.</p>

<div><p><b>Background: </b>Studies on incident liver and cardiovascular outcomes in lean (body mass index: BMI &lt;25 kg/m², or &lt;23 kg/m² for Asians) vs. non-lean individuals with metabolic dysfunction-associated steatohepatitis (MASH) have reported mixed results. We aimed to compare incident clinical outcomes and mortality between lean and non-lean individuals with compensated MASH cirrhosis in a large national cohort.</p>

<div><p><b>Background: </b>Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most common cause of chronic liver disease in the US. Notably, disease prevalence differs greatly by race/ethnicity, with the highest prevalence in those of Hispanic and Asian ancestry, and the lowest prevalence in those of African ancestry. To date, studies have identified common variants associated with MASLD in predominantly European or American populations.

<div><p><b>Background: </b>MAESTRO-NASH (NCT03900429) is an ongoing 54-month, randomized, double-blind, placebo-controlled Phase 3 trial evaluating the efficacy of resmetirom in patients with biopsy-confirmed nonalcoholic steatohepatitis (NASH) and fibrosis. 966 patients with biopsy-confirmed NASH were randomized 1:1:1 to resmetirom 80mg, resmetirom 100mg, or placebo administered once daily. Histologic endpoints were assessed after 52 weeks.

<div><p><b>Background:</p> </b><p>The effect of <em>PNPLA3</em> rs738409 I148M variant (G allele) on the clinical course of adults with biopsy-proven nonalcoholic fatty liver disease (NAFLD) has not been prospectively investigated. We examined (1) the association between <em>PNPLA3</em> G allele and clinical outcomes and (2) how relationships among <em>PNPLA3</em> G allele, age, and type 2 diabetes mellitus (T2DM) impact clinical outcomes in patients with biopsy-proven NAFLD.</p>

<div><p><b>Background: </b>PSC is an archetypical example of a disease with an impaired gut-liver axis and PSC patients with or without inflammatory bowel disease exhibit enteric microbial dysbiosis. Gut microbiota produce diverse metabolic products but how microbes influence PSC disease progression is unclear. By screening bacterial species (sp.) in a transwell gut-liver axis model, we identified novel <em>Leuconostoc sp</em>. (LB-P8) that may have anti-fibrotic properties via inhibition of TGF-β/SMAD signaling.

<div><p><strong><b>Background:</strong> </b>Albumin has been shown to modulate systemic inflammation in patients with decompensated liver cirrhosis receiving infusions of this protein as therapy. Although the anti-inflammatory effect of albumin has been described to be secondary to its internalization into mononuclear leukocytes, the cell type and the mechanism by which albumin is internalized by these immune cells are at present unknown.</p>

<div><p><b>Background: </b>The gut-liver interaction has emerged as a critical component in alcohol-associated liver disease (ALD) pathogenesis. The central mediators are the gut luminal antigens, especially endotoxins that translocate to the liver. This occurs because of (i) compromised gut barrier integrity due to epithelial tight junction (TJ) disruption; and (ii) qualitative/quantitative gut microbiota changes and increased production of pathogenic antigens.</p>

<div><p><strong><b>Background:</strong> </b>Liver fibrosis is the consequence of chronic liver diseases that can progress to cirrhosis and liver failure. However, the role and mechanism of gut leakiness in liver fibrosis are poorly understood, and there is no FDA-approved drug to treat liver fibrosis.

<div><p><b>Background:</p> </b><p>Biliary atresia (BA) is the principal indication for liver transplantation in children, yet there is little information regarding its underlying etiology. Recent data strongly places BA as a developmental cholangiopathy suggesting that there are gene variant contributions that can be discovered using modern gene sequencing and analytical technologies.