Dr. Stephen J. Schillig, Jr. and Mary Schillig Chair in Medicine

Director, Prevention and Lipid Management Program

Professor of Medicine

Professor of Pharmacology

Education

MD - University of Tennessee College of Medicine, 1985
BS - Biology, Tulane University, New Orleans, Louisiana

Postgraduate Training

Internship

Vanderbilt University Medical Center, 1986

Residency

Vanderbilt University Medical Center, 1988

Fellowship

University of California San Francisco Medical Center, 1991

Board and Certifications

Internal Medicine - American Board of Internal Medicine, 1988

Clinical Interest

Areas of Expertise

  • Cardiovascular Medicine
  • Hypercholesterolemia and/or Dyslipidemia
  • Internal Medicine
  • Preventive Cardiology
Research Keywords
Atherosclerosis, Cholesterol, Macrophage, Lipoprotein metabolism, Gene Therapy, Genetics of lipid disorders
Research Description

Dr. Linton is Director of the Vanderbilt Lipid Clinic in the Division of Cardiovascular Medicine and the Atherosclerosis Research Unit. His research programs involve basic science and clinical translational investigations of inherited disorders of lipoprotein metabolism, macrophage biology, and atherosclerosis. Dr. Linton’s early research focused on mutations in the APOB gene that cause inherited low levels of cholesterol. Dr. Linton pioneered the use of bone marrow transplantation (BMT) as an approach to investigate the impact of genes expressed by bone marrow-derived cells, including macrophages, on the development of atherosclerosis in murine models. A major focus of the laboratory is the role of macrophage cholesterol efflux, the first step in reverse cholesterol transport, in atherogenesis. We have a long-standing interest in the roles of apoE, apoA-I, SR-BI, and LRP in lipoprotein metabolism, macrophage cholesterol homeostasis and HDL function. The mechanism of formation of dysfunctional HDL in familial hypercholesterolemia is a focus of our current Program Project Grant on HDL Function in Human Disease. Dr. Linton has recently discovered a critical role for macrophage expression of SR-BI in autophagy in the setting of atherosclerosis.