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.

Areas of Specialty

Pulmonary hypertension: Role of endothelial and vascular smooth muscle oxidant signaling

Achievements & Awards

Dr. Resta has built an NIH-funded research program that has appreciated broad-based recognition by the national and international scientific community, exemplified by service on a variety of NIH and American Heart Association study sections, associate editor and editorial board memberships, selection as a Fellow of the American Heart Association, as Fellow of the American Physiological Society, invited seminars and symposia, and leadership roles on national science committees. 

Dr. Resta has also made meritorious contributions to graduate, medical and undergraduate education and junior faculty development at UNM. He has served in many curriculum development and educational administrative positions at the UNM Health Sciences Center, including Chair of the Cardiovascular/Pulmonary/Renal Block in the Phase I medical curriculum, director of several Biomedical Sciences Graduate Program (BSGP) courses, and a member of both BSGP and MD/PhD steering committees. Nationally he serves on advisory boards for NIH diversity training programs in research education.

His former undergraduate, graduate and postdoctoral trainees have been highly successful in obtaining extramural training fellowships, both mentored and independent NIH grants, and industry, government and faculty-level academic positions. In addition, he is the principle investigator of an NIH-funded T32 Minority Institutional Research Training Grant that supports both pre-doctoral and post-doctoral trainees from diverse ethnic and socio-economic backgrounds.

He has been actively involved as a mentor and teacher in our BSGP, MD/PhD program, and medical curriculum for many years, and has received the School of Medicine’s Faculty Teaching Excellence Award for his contributions to both the BSGP and Phase I medical curriculum. In 2017, he was presented the William G. Dail Award for outstanding and lasting contributions as a teacher, mentor and leader in the medical and graduate education programs at the UNM School of Medicine. Most recently, he was awarded the Faculty Research Excellence Award for Basic Science Research, the highest research recognition award here at the Health Sciences Center.

Key Publications

  • Snow JB, Norton CE, Sands SA, Weise-Cross L, Yan S, Herbert LM, Sheak JR, Gonzalez Bosc LV, Walker BR, Kanagy NL, Jernigan NL, Resta TC. Intermittent hypoxia augments pulmonary vasoconstrictor reactivity through PKCb/mitochondrial oxidant signaling. Am J Respir Cell Mol Biol. 62(6):732-746, 2020.
  • Norton CE, Weise-Cross L, Ahmadian R, Yan S, Jernigan NL, Paffett ML, Naik JS, Walker BR, Resta TC. Altered lipid domains facilitate enhanced pulmonary vasoconstriction following chronic hypoxia. Am J Respir Cell Mol Biol. 62(6):709-718, 2020. (Associated Editorial: Grimmer B, Kuebler WM. Cholesterol – a novel regulator of vasoreactivity in pulmonary arteries. Am J Respir Cell Mol Biol. 62(6):671-673, 2020.)
  • Sheak JR, Yan S, Weise-Cross L, Ahmadian R, Walker BR, Jernigan NL, Resta TC. PKCb and reactive oxygen species mediate enhanced pulmonary vasoconstrictor reactivity following chronic hypoxia in neonatal rats. Am J Physiol. 318 (2), H470-H483, 2020. (APSselect Award for distinction in scholarship)
  • Norton CE, Sheak JR, Yan S, Weise-Cross L, Jernigan NL, Walker BR, Resta TC. Augmented pulmonary vasoconstrictor reactivity following chronic hypoxia requires Src kinase and epidermal growth factor receptor signaling. Am J Respir Cell Mol Biol. 62(1):61-73, 2020. (Associated Editorial: Gao Y, Raj JU. Src and EGFR: Novel partners in mediating chronic hypoxia-induced pulmonary artery hypertension. Am J Respir Cell Mol Biol. 62(1):5-7, 2020.)




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.