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The Hepatobiliary Pathophysiology [HBPP] study section reviews applications involving pathophysiology and treatment of inherited and acquired viral and non-viral hepatobiliary diseases; molecular and genetic regulation of liver development and biochemical function under physiologic and pathophysiologic states; mechanisms of liver injury, repair, regeneration, fibrosis, cancer and transplantation; liver cell biology, immunology and inflammation; cholesterol and bile salt metabolism; hepatic fatty acid and triglyceride metabolism, insulin and hormone signaling, hepatobiliary transporters, hepatic protein metabolism, ion channels; and alcohol metabolism and disease. HBPP study section focuses on both animal models and clinical work.

The List of Reviewers lists all present, whether standing members or temporary, to provide the full scope of expertise present on that date. Lists are posted 30 days before the meeting and are tentative, pending any last minute changes.

Review Dates

Membership Panel

The membership panel is a list of chartered members only.


  • The use of isolated parenchymal and non-parenchymal cells of the liver including hepatocytes, stellate cells, Kupffer cells, endothelial cells, cholangiocytes and resident lymphocytes particularly as they relate to the pathogenesis of liver disease.
  • Progenitor and stem cell therapies of genetic and acquired hepatobiliary diseases.
  • Mechanisms of bile formation, bile salt synthesis hepatic cholesterol and lipid metabolism and their genetic and molecular regulation of cholestatic and gallstone disease.
  • Molecular genetics and biochemical basis for NAFLD and NASH and approaches to intervention and reversal.
  • Physiologic mechanisms of hepatobiliary transport including mechanisms of uptake and excretion of organic solutes, heavy metals, and ions.
  • Inflammatory response of the liver to injury or infection, pro- and anti-inflammatory mediators, oxidative stress and ER stress, apoptosis and autophagy.
  • Mechanism of hepatocyte injury including immune response, oxidative stress, apoptosis, pro- and anti-inflammatory mediators, including signal transduction pathways and neuromediators.
  • Liver development, injury, repair, regeneration, growth, differentiation, development, and aging;
  • Hepatocyte and cholangiocyte dysplasia and pre-neoplasia; mechanisms of transformation; cellular immortalization and mutagenesis.
  • Liver cell and organ transplantation, liver ischemia-reperfusion injury and application of transplantation to the therapy of liver diseases.
  • Regulation of splanchnic blood flow and endothelial vascular function as it pertains to mechanisms of portal hypertension.
  • Cellular and molecular mechanisms of liver diseases, such as, fibrosis and cirrhosis including complications such as ascites and hepatic encephalopathy.
  • Viral hepatitis as it relates to the pathogenesis of hepatobiliary disease.
  • Pathogenesis of alcoholic liver injury, including the role of nutrient deficiencies and endotoxemia.

Shared Interests and Overlaps

There are shared interests with Xenobiotic and Nutrient Disposition and Action (XNDA). Applications concerning drug or herbal-induced liver injury or alcohol-drug interactions are best reviewed by XNDA. Applications that focus on the pathogenesis of alcoholic liver injury and other liver diseases should be assigned to HBPP.

There are shared interests with Integrative Nutrition and Metabolic Processes (INMP) Applications focused on cholesterol and lipid metabolism on liver development and diseases may be assigned to HBPP whereas applications focused on metabolic processes may be assigned to INMP.

There are shared interests with Virology A and Virology B (VIRA & VIRB). Applications concerning the cellular and molecular biology of HBV/HCV viral replication: attachment and entry; gene expression and regulation; viral genome replication; viral assembly and maturation; egress should go to VIRA & VIRB. Applications that focus on liver pathology, liver cell autophagy or necroptosis associated with viral infection may be assigned to HBPP.