<div><p><b>Background:</p> </b><p>Non-alcoholic steatohepatitis (NASH) is prevalent, yet lacks for effective treatments to hinder rapid fibrosis progression, which is the main factor that limits patient prognosis. The role of Hypoxia-inducible factor 1α (HIF-1α) in NASH progression remains unclear. This study investigates the impact and mechanism of hepatocyte-specific HIF-1α deletion on NASH fibrosis, aiming to uncover a novel therapeutic target.</p>

<div><p><strong><b>Background:</strong> </b>osteopontin (OPN, encoded by <em>SPP1</em>) is involved in chronic liver disease. Previous studies reported that intestinal OPN regulates the gut microbiota, however the role of intestinal epithelial cell (IEC)-derived OPN in metabolic dysfunction-associated steatohepatitis (MASH) is unknown.</p>

<div><p><b>Background:<span> </b>Macroautophagy (referred to as autophagy hereafter) is a major intracellular lysosomal degradation pathway that is responsible for the degradation of misfolded/damaged proteins and organelles. Previous studies showed that autophagy protects against acetaminophen (APAP)-induced injury (AILI) via selective removal of damaged mitochondria and APAP protein adducts.

<div><p><strong>Background</strong>: Although nucleotide analogs (NA) prevent viral replication in chronic hepatitis B (CHB) patients, it rarely achieve HBsAg seroclearance. While the reduction of HBsAg levels is associated with HBsAg seroclearance, the factors regulating HBsAg levels are not well understood. To aim for “Functional Cure”, we explored the host immunodynamics involved in the reduction of HBsAg levels.

<div><p><b>Background:</p> </b><p>Portal hypertension progression can be relieved after controlling the etiology of liver cirrhosis. Whether beta-blockers could additionally enhance the effects during treatment, particularly for mild esophageal varices (EVs), was unclear. This study aims to assess the efficacy of add-on carvedilol to delay EVs progression during anti-HBV treatment in HBV-related cirrhosis.</p>

<div><p><b>Background: </b>We and others have shown that rare bi-allelic loss-of-function<strong> </strong>mutations in Kinesin family member 12 (<em>KIF12</em>) cause pediatric high-GGT cholestasis as well as fibrosis, ductular reaction, and bile duct loss. KIF12 has putatively been defined as a microtubule-associated motor protein, but little is known about its function and even less about its role in the pathogenesis of cholestasis.</p>

<div><p><strong><b>Background:</strong> </b>There are very limited high-quality data from which to derive therapeutic approaches to portal hypertension (PHT) in children. Management of varices, in particular, is quite controversial in pediatrics. IMPPHR was developed to derive large-scale international data, thereby enhancing our knowledge of PHT.

<div><p><b>Background:</p> </b><p>Primary sclerosing cholangitis (PSC),<span> </span>a chronic cholangiopathy, results in cholestasis, inflammation, and stricturing of intrahepatic and extrahepatic bile ducts. Recently, we have shown that the transcription factor STAT3 mediated, in part, the protective role of the FXR agonist, GW4064, in parenteral nutrition (PN)-associated cholestasis <em>(Ghosh et al., Hep comm 2023)</em>.

<div><p><b>Background: </b>Hepatorenal syndrome type 1 (HRS-1) is a rapidly progressive form of renal failure associated with high mortality in patients (pts) with decompensated cirrhosis and ascites. The FDA-approved vasopressin analogue, terlipressin (terli), improves renal function in pts with HRS-1 by reducing portal hypertension and increasing effective arterial volume and mean arterial pressure (MAP)—a marker of the hemodynamic response to treatment.

<div><p><strong><b>Background:</strong> </b><span> </span><span> </span>Since our first pediatric anonymous non-directed live donor liver transplant (Anon-LDLT) performed in April 2005, 62 children have undergone live donor liver transplant (LDLT) with an anonymous non-directed graft. Anon-LDLT organs being allocated as per our deceased donor liver transplant wait list.