Robert H. Cox

Robert Cox, PhD, is Professor and Director of Scientific Administration for the Lankenau Institute for Medical Research (LIMR), an independent, hospital-based biomedical research facility located just outside of Philadelphia, in Wynnewood, Pa. LIMR is a division of Main Line Health. He is also an Emeritus Professor of Physiology at the University of Pennsylvania School of Medicine. Dr. Cox has authored and coauthored more than 130 publications, including 22 book chapters on topics related to cardiovascular function in health and disease. His research is focused on how ion channels regulate blood pressure and the electrical signals that drive heartbeat, specifically a type of calcium channel that is present only in arteries. He is a past recipient of the Senior Investigator Achievement Award from the American Heart Association

Dr. Cox earned his B.S. in Electrical Engineering and his M.S. in Biomedical Engineering, both from Drexel University, Philadelphia. His PhD in Biomedical Engineering was awarded at the University of Pennsylvania.

From 1967 to 2000, Dr. Cox served in roles of increasing responsibility at the University of Pennsylvania’s Department of Physiology. He taught primarily Physiology 100, a course taken by all first-year medical students and many graduate students. For most of his tenure, he was responsible for all of the cardiovascular lectures in the course, thus contributing to the training of several thousand future physicians. He also held an appointment in Penn’s Bioengineering Department. While at Penn, Dr. Cox won numerous travel awards and departmental teaching awards.

In addition to his roles at Penn, Dr. Cox served as the Director of the Bockus Research Institute at the Graduate Hospital of the University of Pennsylvania from 1980 to 1997. In that position, he was responsible for the development of an independent biomedical research, and he recruited a vertically integrated group of young investigators in the area of arterial smooth muscle physiology. In 1989, he was also appointed as Director of Research and Scientific Development for Graduate Hospital, where he was responsible for cardiovascular, respiratory and brain research. During that period, the hospital obtained a designation and funding as a Center of Excellence in Cardiovascular Studies from the Ben Franklin Partnership. He also held an appointment as Adjunct Associate Professor of Biomedical Engineering and Science at Drexel University from 1981 to 1992.

Dr. Cox received the prestigious Senior Investigator Achievement Award from the American Heart Association in 1995.

In 2000, he brought his lab to LIMR, where he serves today as a Professor and Director of Scientific Administration. He studies cardiovascular diseases and the effects of disorders that include hypertension, atherosclerosis, Smith-Lemli-Opitz syndrome, short QT syndrome and sudden cardiac death. His research is focused on how ion channels regulate blood pressure and the electrical signals that drive heartbeat, with emphasis on the remodeling of calcium channel in arteries associated with high blood pressure. Calcium channels are microscopic molecular mechanisms that regulate the flow of calcium across cell membranes. By targeting the special type of calcium channel found exclusively in blood vessels, not found in heart muscle, Dr. Cox’s research may lead to the development of more effective, safe and selective therapy against high blood pressure.

More recently, Dr. Cox has been working with others in LIMR and sister institutions to determine how damage to heart muscle associated with reversal of coronary artery block can be prevented. When flow to the heart is restored after a coronary artery blockage, certain protein enzymes called matrix metalloproteases are activated that damage heart muscle cells. Dr. Cox and his coworkers are testing proprietary molecules that target and prevent activation of these enzymes as therapies to help prevent damage and maintain healthy hearts.

Over the years, his research has been supported by the National Institutes of Health, and Pennsylvania Department of Health, as well as private foundations, including the W.W. Smith Charitable Trust, American Heart Association, and American Diabetes Association.

Cox RH, Fromme S (2016). “Functional expression profile of voltage-gated K+ channel subunits in rat small mesenteric arteries.” Cell Biochem Biophys. 74(2):263-76. doi: 10.1007/s12013-015-0715-4.
Cox RH, Fromme S (2015). “Expression of calcium channel subunit variants in small mesenteric arteries of WKY and SHR.” Am J Hypertens. 28(10):1229-39. doi: 10.1093/ajh/hpv024.
Guo D, Yu M, Liu Q, Cox RH, Liu T, Yan GX (2014). “Ventricular hypertrophy amplifies transmural dispersion of repolarization by preferentially increasing the late sodium current in endocardium.” J Electrocardiol. 47(5):642-8. doi: 10.1016/j.jelectrocard.2014.04.004.
Cox RH, Fromme SJ (2013). “A naturally occurring truncated Cav1.2 α1-subunit inhibits Ca2+ current in A7r5 cells.” Am J Physiol Cell Physiol. 305(8):C896-905. doi: 10.1152/ajpcell.00217.2013.
Ren G, Jacob RF, Kaulin Y, Dimuzio P, Xie Y, Mason RP, Tint GS, Steiner RD, Roullet JB, Merkens L, Whitaker-Menezes D, Frank PG, Lisanti MP, Cox RH, Tulenko TN (2011). “Alterations in membrane caveolae and BKCa channel activity in skin fibroblasts in Smith-Lemli-Opitz syndrome.” Mol Genet Metab. 104(3):346-55. doi: 10.1016/j.ymgme.2011.04.019.
Guo DL, Lian JF, Liu TX, Cox RH, Margulies KB, Kowey PR, Yan GX (2011). “Contribution of late sodium current (INa,L) to rate adaptation of ventricular repolarization and reverse use-dependence of QT prolonging agents.” Heart Rhythm. 8(5):762-9. doi: 10.1016/j.hrthm.2010.12.026.
Sun T, Quan XQ, Fromme S, Cox RH, Zhang P, Zhang L, Guo D, Guo J, Patel C, Kowey PR, Yan GX (2011). “A novel mutation in the KCNH2 gene associated with short QT syndrome.” J Mol Cell Cardiol. 50(3):433-41. doi: 10.1016/j.yjmcc.2010.11.017.
Sun Y, Quan XQ, Fromme S, Cox, RH, Zhang L, Zhang P, Guo J, Kowey PR, Yan GX (2010). “A novel mutation in the KCNH2 gene associated with short QT syndrome.” J Mol Cell Cardiol. 50(3):433-41. doi: 10.1016/j.yjmcc.2010.11.017.
Cox RH and Lozinskaya IM (2008). “Ca2+ channel inactivation in small mesenteric arteries of WKY and SHR.” Am J Hyperten. 21:406-412. doi: 10.1038/ajh.2007.73.
Cox RH, Fromme SF, Folander K, R Swanson R (2008). “Voltage gated K+ channel expression in arteries of Wistar Kyoto and spontaneously hypertensive rats.” Am J Hyperten. 21:213-218, doi: 10.1038/ajh.2007.44
Cox RH, Petrou S (1999). “Ca2+ influx inhibits voltage-dependent and augments Ca2+-dependent K+ currents in arterial myocytes.” Am J Physiol (Cell). 277: C51-C63.
Cox RH, Haas KS, Moisey DM, Tulenko TN (1989). “Effects of endothelium regeneration on canine coronary artery function.” Am J Physiol. 257: H1681-H1692.
Cox RH, Bagshaw RJ (1988). “Effect of hypertension and its reversal on canine arterial wall properties.” Hypertension. 12: 301-309.
Cox RH (1981). “Basis for the altered arterial wall mechanics in the spontaneously hypertensive rat.” Hypertension. 3: 485-495.

“Recent Advances in Arterial Diseases: Atherosclerosis, Hypertension and Vasospasm,” ed. Thomas N. Tulenko and Robert H. Cox (New York: Alan R. Liss, Inc.), 1986.
"Acute Myocardial Infarction: Emerging Concepts of Pathogenesis and Treatment,” ed. Robert H. Cox (New York: Praeger), 1989.
"Cellular and Molecular Mechanisms in Hypertension,” ed. Robert H. Cox (New York: Plenum Press), 1989.