Steven J. Sollott, M.D.
Laboratory of Cardiovascular Science
251 Bayview Boulevard
Baltimore, MD 21224
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.
Cortassa S, Sollott SJ, Aon MA. Mitochondrial respiration and ROS emission during β-oxidation in the heart: An experimental-computational study. PLoS Comput Biol. 2017;13(6):e1005588.
Zorov DB, Juhaszova M, Sollott SJ. Mitochondrial reactive oxygen species (ROS) and ROS-induced ROS release. Physiol Rev. 2014;94(3):909-50.
Yaniv Y, Juhaszova M, Wang S, Fishbein KW, Zorov DB, Sollott SJ. Analysis of mitochondrial 3D-deformation in cardiomyocytes during active contraction reveals passive structural anisotropy of orthogonal short axes. PLoS One. 2011;6(7):e21985.
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.
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.
Related Scientific Focus Areas
Biomedical Engineering and Biophysics
This page was last updated on August 20th, 2018