Steven J. Sollott, M.D.

Senior Investigator

Laboratory of Cardiovascular Science


251 Bayview Boulevard
Suite 100
Baltimore, MD 21224


Research Topics

We are studying structure and function of cells from the cardiovascular system along two principal and distinct lines: 1) mechanisms of cardiac contractility, and 2) cellular changes after vascular injury. An underlying theme in both of these areas involves the pursuit and development of single cell biophysical methods to overcome certain limitations and complexities inherent in in vivo and in multicellular in vitro experimental systems, to gain an understanding of basic cell biological processes that may have implications for the pathophysiology and treatment of human disease.


Dr. Sollott received his M.D. from the University of Rochester and completed his residency in internal medicine at a Cornell University program. He subsequently completed his cardiology fellowship at Johns Hopkins University and an NIH medical staff fellowship at NIA's Laboratory of Cardiovascular Science. His research attempts to bridge interests spanning basic and clinical science to therapeutics.

Selected Publications

  1. Aon MA, Cortassa S, Juhaszova M, González-Reyes JA, Calvo-Rubio M, Villalba JM, Lachance AD, Ziman BD, Mitchell SJ, Murt KN, Axsom JEC, Alfaras I, Britton SL, Koch LG, de Cabo R, Lakatta EG, Sollott SJ. Mitochondrial health is enhanced in rats with higher vs. lower intrinsic exercise capacity and extended lifespan. NPJ Aging Mech Dis. 2021;7(1):1.

  2. Cortassa S, Sollott SJ, Aon MA. Mitochondrial respiration and ROS emission during ╬▓-oxidation in the heart: An experimental-computational study. PLoS Comput Biol. 2017;13(6):e1005588.

  3. Zorov DB, Juhaszova M, Sollott SJ. Mitochondrial reactive oxygen species (ROS) and ROS-induced ROS release. Physiol Rev. 2014;94(3):909-50.

  4. Juhaszova M, Zorov DB, Kim SH, Pepe S, Fu Q, Fishbein KW, Ziman BD, Wang S, Ytrehus K, Antos CL, Olson EN, Sollott SJ. Glycogen synthase kinase-3beta mediates convergence of protection signaling to inhibit the mitochondrial permeability transition pore. J Clin Invest. 2004;113(11):1535-49.

  5. Zorov DB, Filburn CR, Klotz LO, Zweier JL, Sollott SJ. Reactive oxygen species (ROS)-induced ROS release: a new phenomenon accompanying induction of the mitochondrial permeability transition in cardiac myocytes. J Exp Med. 2000;192(7):1001-14.

This page was last updated on August 19th, 2021