Clint L. Miller, Ph.D.

My laboratory’s research focus involves the application of modern genomics to unravel complex human diseases. By integrating large-scale human genetic association data with multi-omic profiling and functional models, our work seeks to better understand causal disease mechanisms. We are interested in dissecting the role of genetic and drug perturbations on vascular wall processes during atherosclerosis progression. We are also interested in studying gene-gene and gene-environment interactions at the molecular level to further inform translational targeting of multiple risk loci.

Assistant Professor, Public Health Sciences
Center for Public Health Genomics
P.O. Box 800717
Tel: 1-434-982-0502
Fax: 1-434-982-1815
Email: clintm@virginia.edu
Health System West Complex, Room 3231

Education and Training:

Postdoctoral Fellowship, Human Genetics, Stanford University, 2011-2015
Ph.D., Pharmacology, University of Rochester, 2011
M.S., Pharmacology, University of Rochester, 2007
B.S., Neuroscience, University of Maryland, Baltimore County, 2003

Research Interests:

Genetic variation, Complex diseases, Coronary artery disease, Regulatory mechanisms, Epigenomics, Vascular biology and physiology

Other Appointments:

Links to More Information:

Selected Publications:

Miller 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, Franzen O, Assimes TL, Montgomery SB, Schadt EE, Björkegren J, Quertermous T. Integrative functional genomics identifies regulatory mechanisms at coronary heart disease loci. Nature Communications. 2016 Jul 8;7:12092.

Miller CL, Haas U, Diaz R, Leeper NJ, Kundu RK, Patolla B, Assimes TL, Kaiser FJ, Ljubica P, Hedin U, Maegdefessel L, Schunkert H, Erdmann J, Quertermous T, Sczakiel G. Coronary heart disease-associated variation in TCF21 disrupts a miR-224 binding site and miRNA-mediated regulation. PLOS Genetics. 2014 Mar 27; 10(3):e1004263.

Miller CL, Assimes TL, Montgomery SB, Quertermous T. Dissecting the causal genetic mechanisms of coronary heart disease. Current Atherosclerosis Reports. 2014 May;16(5):406.

Miller 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. Disease-related growth factor and embryonic signaling pathways modulate an enhancer of TCF21 expression at the 6q23.2 coronary heart disease locus. PLOS Genetics. 2013 Jul;9(7):e1003652.

Miller CL, Oikawa M, Cai Y, Thomas T, Dostmann W, Zaccolo M, Fujiwara K, Yan C. Cyclic nucleotide phosphodiesterase 1: a key regulator of cardiac fibroblast activation and extracellular matrix remodeling in the heart. Basic Research in Cardiology. 2011 Nov;106(6): 1023-39.

Miller CL, Oikawa M, Cai Y, Wojtovich AP, Nagel DJ, Xu X, Xu, H, Rybalkin SD, Beavo JA, Chen YF, Li JD, Blaxall BC, Abe J, Yan C. Role of Ca2+/CaM-stimulated phosphodiesterase 1 in mediating cardiomyocyte hypertrophy. Circulation Research. 2009 Nov 6;105(10): 956-64.

See complete list of publications on Pubmed or Google Scholar.