Mary Sorci-Thomas, PhD

Mary G. Sorci-Thomas, PhD

Professor; Associate Director, Cardiovascular Center; Program Director, CVC T32 Training Program


  • Endocrinology

Contact Information

General Interests

Lipid Metabolism, Atherosclerosis, Obesity, Adipocyte Biology


BS, Louisiana State University, Baton Rouge, LA
PhD, Wake Forest University School of Medicine, Winston-Salem, NC


Secondary Appointments

  • Associate Director Cardiovascular Center
  • Program Director, CVC T32 Training Program

Mary Sorci-Thomas PhD, is a Professor of Medicine in the Division of Endocrinology, Metabolism and Clinical Nutrition and an Associate in the Department of Pharmacology and Toxicology at the Medical College of Wisconsin (MCW) in Milwaukee, WI. She is currently an Associate Director of the Cardiovascular Center and Associate Program Director for the CVC T32 Training Program. She also holds a Senior Adjunct Investigator at the Versiti Blood Research Institute. Dr. Sorci-Thomas grew up in New Orleans, Louisiana and graduated from Louisiana State University in Baton Rouge with a BS degree in Biochemistry and Chemistry. She then pursued her PhD in Biochemistry at Wake Forest University in Winston-Salem, NC. In 1984 she was awarded a National Research Service Award Fellowship from the National Institute of Health to study Molecular Biology at the State University of New York at Stony Brook. After completing her fellowship she joined the Wake Forest University Medical School Department of Pathology in 1987 where she rose through the ranks becoming a Professor with Tenure in 2002. During her career at Wake Forest she was awarded an Established Investigatorship from the American Heart Association in 1994. She also served as a Charter Members for both the Metabolism Study Section and Program Project Study Section for the National Heart Lung and Blood Institute of the NIH. In December of 2014 Dr. Sorci-Thomas moved to the Medical College of Wisconsin to join the Department of Medicine and the Cardiovascular Research Center. Her research focuses on HDL Metabolism as it pertains to Diabetes, Obesity and Cardiovascular Health. She has been continuously funded for over 33 years by the National Institutes of Health and for 20 years participated as a Project Leader on an NIH funded Program Project that studied Atherosclerosis and Lipid Metabolism. She serves on the Editorial Board for the Journals of Arteriosclerosis, Thrombosis and Vascular Biology (ATVB) and the Journal of Lipid Research and is a Charter Member of the Molecular and Cellular Endocrinology Study Section of the NIH. She has given over 100 research seminars both nationally and internationally, and written over 90 peer-reviewed articles. During her career she has consistently volunteered for various roles associated with the American Heart Association and in 1999 received the Mentor of Women award from the ATVB Council. Currently, she serves as Chair of the Council on Atherosclerosis, Thrombosis and Vascular Biology for the American Heart Association.

Leadership Positions


  • Member, American Heart Association Council Operations Committee
  • Immediate-Past Chair, American Heart Association Council on Atherosclerosis, Thrombosis and Vascular Biology
  • Chair, American Heart Association Atherosclerosis, Thrombosis and Vascular Biology Council Nominations Committee
  • Member American Heart Association, Atherosclerosis, Thrombosis and Vascular Biology Spring Meeting Program Committee
  • Editorial Board, Journal of Lipid Research
  • Editorial Board, Atherosclerosis, Thrombosis and Vascular Biology Journal
  • Board of Directors, Kern Lipid Conference
  • Editorial Board, Circulation Research
  • Associate Editor, Atherosclerosis Plus
  • Specialty Chief Editor, Lipids in Cardiovascular Disease-Frontiers in Cardiovascular Medicine

MCW Internal

  • Associate Director Cardiovascular Center (CVC)
  • Associate Director Cardiovascular Center T32 Training Grant
  • Chair, Cardiovascular Center Space and Equipment Committee
  • Member, MCW Mentoring Committees

Research Experience

  • Atherosclerosis
  • Cholesterol, HDL
  • Macrophages
  • Stem Cells
  • Vascular Endothelial Growth Factors

Research Interests

Dr. Sorci-Thomas’ research interests have recently expanded to include the study of obesity, lipid metabolism and cardiovascular disease. Prior to this, her work focused mainly on the cardiovascular disease as it relates to the biochemistry and physiology of HDL apoA-I. Much of this work was aimed at solving the structure and function of the main HDL protein constituient apoA-I. Two papers which provide examples of this work:

  • Sorci-Thomas, MG., Thomas, MJ. 2002. The effects of altered apolipoprotein A-I structure on plasma HDL concentration. In: Trends Cardiovas Medicine. 12:121-28
  • Melchior JT, Walker RG, Cooke AL, Morris J, Castleberry M, Thompson TB, Jones MK, Song HD, Rye KA, Oda MN, Sorci-Thomas MG, Thomas MJ, Heinecke JW, Mei X, Atkinson D, Segrest JP, Lund-Katz S, Phillips MC, Davidson WS. 2017. A consensus model of human apolipoprotein A-I in its monomeric and lipid-free state. Nat Struct Mol Biol. 12:1093-1099

As the HDL field matured, it became evident that the main protein constituient of HDL, apoA-I, acted as an anti-inflammatory molecule by regulating the amount of plasma membrane or lipid raft cholesterol via efflux mechanisms. This process suppresses inflammatory signaling pathways thereby modulating monocyte influx into the artery wall. These interests led to several important discoveries which can be summarized by two of the following papers:

  • Sorci-Thomas, MG, Thomas, MJ. 2016 Microdomains, Inflammation and Atherosclerosis. Circ Res 118:679-91
  • Gaddis, DE, Padgett, LE, W, R, McSkimming, C, Romines, V, Taylor, AM, McNamara, CA, Kronenberg M, Crotty S, Thomas, MJ, Sorci-Thomas, MG, Hedrick, CC. .2018. Apolipoprotein AI prevents regulatory to follicular helper T cell switching during atherosclerosis. Nat Comm. March 15;9(1):1095

Now that was appreciated that expression of lipid-free apoA-I influenced the activation status of immune cells through modulation of lipid raft cholesterol, additional studies were carried out to examine how apoA-I modulated signaling in lymphocytes in inflammatory states two examples of this work include:

  • Wilhelm, AJ, Zabalawi, M, Shah, D, Owen, JS, Grayson, JM, Major, AS, Bhat, S. Gibbs, Jr, DB, Thomas, MJ, Sorci-Thomas, MG. 2010. Apolipoprotein A-I Results in Increased Regulatory T Cells and Decreased T Cell Activation in Lymph Nodes and Reversal of Lipid Accumulation in the Skin of Diet-fed LDLr-/-, ApoA-I-/-Mice. J Biol Chem 285:36158-69
  • Potteaux, S, Gautier, EL, Hutchison, SB, van Rooijen, N, Rader, DJ, Thomas, MJ, Sorci-Thomas. MG, Randolph, GJ. 2011. Suppressed monocyte recruitment drives macrophage removal from atherosclerotic plaques of ApoE-/- mice during disease regression. J Clin Invest 121:2025-36.

Laboratory Studies

  • Obesity
  • Cardiovascular Disease
  • Adipocyte Biology
  • Lipid Metabolism
  • Lipoprotein Metabolism