Dr. Resta received his Ph.D. in 1995 from UNM and remained as a postdoctoral fellow before joining the Cell Biology & Physiology faculty as a research assistant professor in 1998. He was promoted to assistant professor in 2000, associate professor in 2006, and professor in 2012. In 2020 was named the senior associate dean for research education at the UNM School of Medicine.

Key Publications

Journal Article
Norton, C, E Jernigan, Nikki, Walker, B, R Resta, Tom, 2020 Membrane depolarization is required for pressure-dependent pulmonary arterial tone but not enhanced vasoconstriction to endothelin-1 following chronic hypoxia. Pulmonary circulation, vol. 10, Issue 4, 2045894020973559
Journal Article
Yan, S, Resta, Tom, Jernigan, Nikki, 2020 Vasoconstrictor Mechanisms in Chronic Hypoxia-Induced Pulmonary Hypertension: Role of Oxidant Signaling. Antioxidants (Basel, Switzerland), vol. 9, Issue 10


Dr. Resta’s current research program involves two main projects that examine the contribution of inflammation and oxidant signaling to pulmonary hypertension (pHTN). The first is to identify vascular smooth muscle (VSM) signaling mechanisms responsible for PKC and mitochondrial reactive oxygen species (ROS)-mediated pulmonary vasoconstriction, and to define the role of this signaling pathway in chronic intermittent hypoxia (CIH)-dependent increases in vasoconstrictor reactivity, arterial remodeling and associated pHTN in a clinically relevant rodent model of sleep apnea. The second project examines mechanisms by which chronic sustained hypoxia mediates pressure-dependent pulmonary VSM tone, augments vasoconstrictor reactivity, and their contribution to the development of pHTN. These mechanisms involve inflammation-associated activation of a Src kinase/EGFR signaling mechanism in pulmonary VSM that confers mechanical, electrical and chemical transduction to NADPH oxidase-derived O2- production, RhoA-mediated vasoconstriction, arterial remodeling and pHTN.