B.S. Neuroscience, University of Maryland Baltimore County, 2003M.S. Pharmacology, University of Rochester, 2007Ph.D. Pharmacology, University of Rochester, 2011 Postdoc Human Genetics, Stanford University, 2015
"We leverage natural genetic variation and data-driven approaches to identify new risk factors and treatments for cardiovascular disease."
Clint Miller studies the genetic and environmental risk factors for coronary artery disease and other complex cardiovascular diseases using a combination of large-scale multi-omics profiling and genetic and drug perturbations. He is an Assistant Professor in Public Health Sciences and a resident member of the Center for Public Health Genomics. He is also a member of the Data Science Institute, Robert Berne Cardiovascular Institute, and holds secondary appointments in Biomedical Engineering and Biochemistry and Molecular Genetics. He joined UVA in 2017.
Clint was previously an Instructor at Stanford University in Cardiovascular Medicine from 2015-2017. He earned his PhD in Pharmacology at the University of Rochester with Chen Yan investigating cyclic nucleotide signaling pathways in the heart and completed his postdoctoral fellowship in human genetics and genomics at Stanford University with Tom Quertermous. There he investigated the regulatory mechanisms of coronary artery disease loci identified from genome-wide association studies. The Miller Lab studies the genetic and environmental risk factors for coronary artery disease and other complex cardiovascular diseases using a combination of large-scale multi-omics profiling and genetic and drug perturbations. They integrate computational and functional genomic analyses, vascular biology and systems pharmacology approaches to study causal regulatory networks driving the disease process. Their goal is to identify novel markers to better classify patients with cardiovascular disease as well as inform tailored treatments that target dysregulated pathways in the vessel wall.
NIH Pathway to Independence Award
American Heart Association Young Investigator Award
European Atherosclerosis Society Young Investigator Fellowship
TEDMED Front Line Full Scholar Award
American Heart Association Fellowship Award
Biomedical Data Sciences
Computational and Functional Genomics
Cardiovascular Genetics and Biology
Integrative functional genomics identifies regulatory mechanisms at coronary artery disease loci. Nat Comms. 2016 7, 12092. ABSMiller CL, Pjanic M, Wang T, Nguyen T, Cohain A, Lee JD, Perisic L, Hedin U, Kundu RK, Majmudar D, Kim JB, Wang O, Betsholtz C, Ruusalepp A, Franzén O, Assimes TL, Montgomery SB, Schadt EE, Björkegren JL, Quertermous T.
Genetics and genomics of coronary artery disease. Curr Cardiol Rep. 2016 Oct;18(10):102. ABSPjanic M, Miller CL, Wirka R, Kim JB, DiRenzo DM, Quertermous T
CD47-blocking antibodies restore phagocytosis and prevent atherosclerosis. Nature. 2016 536 (7614), 86. ABSKojima Y, Volkmer JP, McKenna K, Civelek M, Lusis AJ, Miller CL, Direnzo D, Nanda V, Ye J, Connolly AJ, Schadt EE, Quertermous T, Betancur P, Maegdefessel L, Matic LP, Hedin U, Weissman IL, Leeper NJ.
Systems Genomics Identifies a Key Role for Hypocretin/Orexin Receptor-2 in Human Heart Failure. J Am Coll Cardiol. 2015 Dec 8;66(22):2522-33. ABSPerez MV, Pavlovic A, Shang C, Wheeler MT, Miller CL, Liu J, Dewey FE, Pan S, Thanaporn PK, Absher D, Brandimarto J, Salisbury H, Chan K, Mukherjee R, Konadhode RP, Myers RM, Sedehi D, Scammell TE, Quertermous T, Cappola T, Ashley EA.
Coronary heart disease-associated variation in TCF21 disrupts a miR-224 binding site and miRNA-mediated regulation. PLoS Genet. 2014 Mar 27;10(3):e1004263. ABSMiller CL, Haas U, Diaz R, Leeper NJ, Kundu RK, Patlolla B, Assimes TL, Kaiser FJ, Perisic L, Hedin U, Maegdefessel L, Schunkert H, Erdmann J, Quertermous T, Sczakiel G.
Dissecting the causal genetic mechanisms of coronary heart disease. Curr Atheroscler Rep. 2014 May;16(5):406. ABSMiller CL, Assimes TL, Montgomery SB, Quertermous T.
Disease-related growth factor and embryonic signaling pathways modulate an enhancer of TCF21 expression at the 6q23.2 coronary heart disease locus. PLoS Genet. 2013;9(7):e1003652. ABSMiller CL, Anderson DR, Kundu RK, Raiesdana A, Nürnberg ST, Diaz R, Cheng K, Leeper NJ, Chen CH, Chang IS, Schadt EE, Hsiung CA, Assimes TL, Quertermous T.