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Wake Forest University School of Medicine
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  • Wake Forest University School of Medicine
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  • Matt Quinn, PhD

Matt Quinn, PhD

  • Assistant Professor, Pathology - Comparative Medicine
Matt Quinn, PhD

Matt Quinn, PhD

  • Assistant Professor, Pathology - Comparative Medicine

Research Interests

  • Obesity
  • Women's Health
  • Fatty Liver
  • Nuclear Receptors
  • Reproduction
  • Epigenesis, Genetic
Education
BA, Texas Tech University, 2008
PhD, Texas A&M University, 2013
Fellowship
Molecular Endocrinology, National Institute of Environm, 2018
Memberships
Endocrine Society
Positions
Assistant Professor, Pathology - Comparative Medicine
Assistant Professor, Molecular Medicine
Departments and Affiliations
Pathology - Comparative Medicine
Molecular Medicine
Cardiovascular Sciences Center
Sticht Center for Healthy Aging and Alzheimer's Prevention
Center on Diabetes, Obesity, and Metabolism
Center for Redox Biology and Medicine
Center for Precision Medicine

Research

  • Publications
  • Silencing of maternal hepatic glucocorticoid receptor is essential for normal fetal development in mice. Quinn MA, McCalla A, He B, Xu X, Cidlowski JA. Commun Biol. 2019; 2:104.
  • Comms Bio. In Press. Quinn MA, McCalla A, He B, Xu X, Cidlowski JA. Silencing of maternal hepatic glucocorticoid receptor is essential for normal fetal development in mice. 2019 Jan; 1;
  • Estrogen Deficiency Promotes Hepatic Steatosis via a Glucocorticoid Receptor-Dependent Mechanism in Mice. Quinn MA, Xu X, Ronfani M, Cidlowski JA. Cell Rep. 2018 03; 22(10):2690-2701.
  • Bile Acid Signaling Is Involved in the Neurological Decline in a Murine Model of Acute Liver Failure. McMillin M, Frampton G, Quinn M, Ashfaq S, de los Santos M, Grant S, DeMorrow S. Am. J. Pathol. 2016 Feb; 186(2):312-23.
  • Endogenous hepatic glucocorticoid receptor signaling coordinates sex-biased inflammatory gene expression. Quinn MA, Cidlowski JA. FASEB J. 2016 Feb; 30(2):971-82.
View More Publications

Research Interests

  • Chromatin
  • Diabetes/Metabolism
  • Energy Metabolism
  • Epigenesis, Genetic
  • Fatty Liver
  • Metabolomics
  • Nuclear Receptors
  • Obesity
  • Reproduction
  • Women's Health

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