The liver is exposed to numerous insults over a person's lifetime, which can drive chronic liver disease. Broadly, the Integrative Biology of Advanced Liver Disease Lab is interested in several aspects of chronic liver disease, including the mechanisms of alcoholic liver disease, how fibrosis and inflammation respond to liver injury and drive fibrogenesis, as well as how endothelial cells in the liver contribute to liver disease.

  • Alcoholic liver disease. A major cause of morbidity and mortality, alcoholic liver disease is one of the leading causes of liver cirrhosis. Our program works on multiple aspects of alcoholic liver disease, including identification of novel genes that contribute to alcoholic liver disease. The lab's clinical work includes treatment trials, development of models for diagnosis and prognosis, as well as epidemiologic and pathophysiologic studies.
  • Nonparenchymal liver cell biology. A crucial role in the development of advanced liver disease is played by nonparenchymal liver cells. These cells include pericytes, endothelial cells and immune cells. While constituting a minority of the total liver architecture, these cells directly contribute to liver disease by promoting fibrosis, portal hypertension and inflammation. Our work endeavors to understand the cellular and molecular mechanisms that facilitate the pathogenic contributions of these cells to liver disease and the identification and development of therapeutic strategies for use in patients.
  • Pathobiology of hepatic extracellular vesicles. In the liver, extracellular vesicles are vital for autocrine and paracrine signaling. In recent years, the pathological role of extracellular vesicles in chronic liver disease has emerged. Our lab studies how pathological changes in extracellular vesicle cargo and release from hepatic stellate cells drives liver fibrosis and the progression of liver disease.
  • Novel therapies for portal hypertension. Portal hypertension is a major complication of liver cirrhosis. Our laboratory has a focus on the cellular and molecular mechanisms of portal hypertension. This includes the relevant signaling pathways in liver endothelial cells and hepatic stellate cells and how these pathways are deranged in response to hepatic injury and fibrosis.