Frank A Anania, MD, AGAF, FACP

R. Bruce Logue Chair and Professor of Medicine

Emory University Department of Medicine

Division Director and Professor of Medicine, Digestive Diseases

Emory University Department of Medicine

Phone: 404-712-2867



Emory Healthcare clinical profile

Dr. Anania has been a faculty member of the two medical schools located in Baltimore: Johns Hopkins School of Medicine and the University of Maryland School of Medicine. His role as a hepatologist in both institutions was three-fold, including the roles of clinician, teacher, and biomedical researcher. In 2001, he became director of Liver Diseases at the University of Maryland. In his role as clinician, he actively cared for patients with liver disease in both institutions' family practice plans. His clinical work included treatment of complications of chronic liver disease, use of drugs for chronic HCV infection, and a multi-disciplinary approach to patients with NAFLD. He has also cared for patients before and after liver transplantation. 

At the University of Pittsburgh, as both an undergraduate and as a medical student, Dr. Anania worked in a biomedical research laboratory. It was at Pittsburgh that, as a medical student, with a burgeoning liver disease population of patients, he became quite interested in liver diseases. Importantly, his exposure to basic biological research focused on connective tissue, or extracellular matrix molecules that support the machinery of each organ system of the human body. For Dr. Anania, the logical approach for an academic career, therefore, was to study why liver patients developed an excess of this connective tissue that leads to scarring, cirrhosis, and even liver cancer. His initial work focused on how by-products of alcohol could induce increased collagen production in stellate cells. Collagen is the primary component of the scarred liver, and stellate cells are primarily responsible for producing collagen and other molecules that destroy normal liver blood flow and function.

At present, Dr. Anania’s laboratory is intensively investigating the molecular role of leptin in the development of liver scarring. They have convincingly demonstrated that leptin is definitely harmful in excess quantities and leads to enhanced liver scar tissue as well as multiplication of stellate cells. Importantly, it acts as a brake to preventing diseased stellate cells from dying, thereby preventing the body’s mechanisms from controlling excess scarring from becoming severe. They are currently using animal models with single-gene deficiencies to gain an understanding of exactly how leptin alters the life cycle of stellate cells, and how it transmits signals to the cell nucleus that result in dangerous events for the health of the liver. Finally, they have begun to look at naturally occurring substances, or peptides made by the human body to determine whether they can prevent or reduce the burden of obesity on the liver and thereby prevent serious liver disease and cirrhosis.  

Two broad areas of active research occur in the laboratory. One focuses on the role of oxidative stress in altering the transcriptional regulation of genes in hepatic stellate cells. The second focus relates to the initial observation made in our laboratory, that leptin, the weight-controlling hormone, is required for liver fibrosis. Recent work also focused on the role of glucagon-like peptides (GLPs), in particular, GLP-1, and its reptilian homologue, Exendin-4, for treatment of non-alcoholic fatty liver diesase (NAFLD). Finally, they are examining the role of leptin in hepatoctye cell cycle kinetics and resistance to apoptosis; properties, among others, that predispose obese humans with an increased of hepatocellular carcinoma.