Tiểu sử

Dr. Resta received his Ph.D. from the UNM School of Medicine in 1995 and continued at UNM on an NIH postdoctoral fellowship until 1998. Following postdoctoral training, he joined the Department of Cell Biology and Physiology as a research assistant professor in 1998, and as a tenure-track assistant professor in 2000 following a national search. He was promoted to Associate Professor with tenure in 2006, and to Professor in 2012. Dr. Resta was appointed Senior Associate Dean for Research Education at the School of Medicine in 2020, Interim Senior Associate Dean for Research in 2022, and was named a Regents' Professor in 2022.

Đơn trình bày nguyện vọng cá nhân (Personal Statement)

Dr. Resta has established a productive NIH-funded research program to understand mechanisms of pulmonary hypertension associated with chronic obstructive lung diseases, sleep apnea, and high-altitude exposure. He has been actively engaged in cardiovascular research since 1990 and has served as PI on multiple NIH R01 grants and other national-level awards over the past 25 years. His research 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. His research accomplishments have been recognized by the Faculty Research Excellence Award for Basic Science Research, the highest research recognition bestowed at the Health Sciences Center. He later received the UNM Regents' Professor Award in 2022, celebrating remarkable contributions across the principal domains of academic pursuit: teaching, scholarly works, and administrative service to the University. In 2024, Dr. Resta received the UNM Faculty Research Award, which recognizes exceptional achievements and significant contributions in research by UNM faculty.

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, as director of several Biomedical Sciences Graduate Program (BSGP) courses, and as 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 Principal 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. Dr. Resta has also been actively involved as a mentor and teacher in our BSGP, MD/PhD program, UPN 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.

As Senior Associate Dean for Research Education, Dr. Resta has led innovative programs in research education, including undergraduate, MS and PhD in Biomedical Sciences, MD/PhD, and the Master of Science in Clinical Research programs at the School of Medicine. He recently developed a new Postdoctoral Affairs program that, in collaboration with the Central Campus Office of the Vice President for Research, provides improved support, oversight, and campus-wide training opportunities for postdoctoral scholars. More recently, Dr. Resta was appointed Interim Senior Associate Dean for Research at the School of Medicine where he leads faculty research education and support programs.

Lĩnh vực chuyên môn

Vascular physiology
Tăng huyết áp động mạch phổi
Vascular smooth muscle and endothelial cell signaling

Thành tựu & Giải thưởng

UNM Faculty Research Award, 2024

UNM Regents’ Professor Award, 2022.

Learning Environment Office Teaching Excellence Recognition Awards, 2020-present.

Faculty Research Excellence Award for Basic Science Research, UNM Health Sciences Center, 2019.

Fellow of the American Physiological Society (FAPS), 2019.

HIPPO Award, Best Lecturer in Phase I as voted by the UNM M.D. Class of 2021.

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, 2017-2020.

Educational Excellence Award for Faculty, Teaching, Phase I Medical Curriculum, UNM School of Medicine, 2014-2015.

Fellow of the American Heart Association (FAHA), Council on Basic Cardiovascular Sciences, 2011; Council on Cardiopulmonary, Critical Care and Resuscitation, 2013.

Educational Excellence Award for Faculty, Teaching, Phase I Medical Curriculum, UNM School of Medicine, 2010-2011.

Fellow of the Pulmonary Vascular Research Institute, 2010.

New Investigator Award, American Physiological Society, Respiration Section, 2005.

Educational Excellence Award for Faculty, Teaching, Biomedical Sciences Graduate Program, UNM School of Medicine, 2004-2005.

Parker B. Francis Fellowship in Pulmonary Research, Harvard School of Public Health, 2000-2003.

Dean’s Award of Distinction in Recognition of Outstanding Faculty Performance, UNM Health Sciences Center, 2000.

Ấn phẩm chính

Bài báo
Norton, C, E Jernigan, Nikki, Walker, B, R Resta, Tom, 2020 Khử cực màng là cần thiết cho trương lực động mạch phổi phụ thuộc áp lực nhưng không tăng cường co mạch thành endothelin-1 sau tình trạng thiếu oxy mãn tính. Tuần hoàn phổi, tập. 10, Số 4, 2045894020973559
Bài báo
Yan, S, Resta, Tom, Jernigan, Nikki, 2020 Cơ chế co mạch trong tăng huyết áp phổi mãn tính do thiếu oxy: Vai trò của tín hiệu oxy hóa. Chất chống oxy hóa (Basel, Thụy Sĩ), vol. 9, Số 10 https://www.mdpi.com/2076-3921/9/10/999

Giới Tính

Nam

Nghiên cứu

Chương trình nghiên cứu hiện tại của Tiến sĩ Resta liên quan đến hai dự án chính kiểm tra sự đóng góp của quá trình viêm và tín hiệu oxy hóa đối với tăng áp động mạch phổi (pHTN). Đầu tiên là xác định cơ chế truyền tín hiệu của cơ trơn mạch máu (VSM) chịu trách nhiệm về sự co thắt mạch máu phổi qua trung gian PKC và ty thể (ROS), và xác định vai trò của con đường truyền tín hiệu này trong sự gia tăng phụ thuộc vào tình trạng thiếu oxy ngắt quãng mạn tính (CIH) trong chất co mạch. khả năng phản ứng, tái tạo động mạch và pHTN liên quan trong mô hình ngừng thở khi ngủ ở động vật gặm nhấm có liên quan về mặt lâm sàng. Dự án thứ hai nghiên cứu các cơ chế mà tình trạng thiếu oxy kéo dài mãn tính làm trung gian cho trương lực VSM phổi phụ thuộc vào áp suất, làm tăng phản ứng co mạch và sự đóng góp của chúng vào sự phát triển của pHTN. Các cơ chế này liên quan đến sự kích hoạt liên quan đến viêm của cơ chế truyền tín hiệu Src kinase / EGFR trong VSM phổi giúp truyền dẫn cơ học, điện và hóa học sang O có nguồn gốc từ NADPH oxidase.2- sản xuất, co mạch qua trung gian RhoA, tái tạo động mạch và pHTN.

khóa học dạy

Course Director and Lecturer, Cardiovascular/Pulmonary/Renal Block, Phase I Medical Curriculum, University of New Mexico School of Medicine

Course Director and Lecturer, Advanced Topics in Cellular and Systems Physiology, University of New Mexico School of Medicine

Course Director, Cardiovascular Biology Journal Club/Seminar, University of New Mexico School of Medicine

Course Director and Lecturer, Graduate Physiology, University of New Mexico School of Medicine

Nghiên cứu và học bổng

Dr. Resta's laboratory employs a wide array of technical approaches to assess mechanisms of pulmonary hypertension, including measurement of hemodynamic variables in conscious, chronically instrumented rats, simultaneous assessment of vasoreactivity and vessel wall [Ca2+]i in isolated, pressurized small pulmonary arteries, and a variety of cellular imaging and molecular approaches to study both Ca2+ and oxidant signaling in vascular endothelial and smooth muscle cells. Below is a link to Dr. Resta's complete published work, along with some representative publications:

Complete List of Published Work (https://pubmed.ncbi.nlm.nih.gov/?term=resta+tc+OR+%28resta+t+AND+bosc+lv+AND+kanagy%29&sort=pubdate)

Chronic hypoxia imparts myogenicity and augments vasoconstriction: role for membrane cholesterol regulation of a novel oxidant signaling pathway in vascular smooth muscle
Weise-Cross L, Sands MA, Sheak JR, Broughton BRS, Snow JB, Gonzalez Bosc LV, Jernigan NL, Walker BR, Resta TC. Actin polymerization contributes to enhanced pulmonary vasoconstrictor reactivity following chronic hypoxia. Am J Physiol. 314:H1011-H1021, 2018. (Associated Editorial: Aaronson PI. Actin polymerization contributes to ROS- and Rho-dependent Ca2+ sensitization in pulmonary arteries from chronic hypoxic rats. Am J Physiol. 515(2):H314-H317, 2018)

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.)

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.)

Yan S, Sheak JR, Walker BR, Jernigan NL, Resta TC. Contribution of mitochondrial reactive oxygen species to chronic hypoxia-induced pulmonary hypertension. Chất chống oxy hóa.12(12):2060, 2023.

Mechanisms of enhanced pulmonary vasoreactivity following chronic intermittent hypoxia (CIH) and in neonatal pulmonary hypertension: role of PKCbeta and mitochondrial ROS (mtROS) signaling
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)

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.

Reduced membrane cholesterol following chronic hypoxia impairs pulmonary endothelial Ca2+ entry: implications for endothelial dysfunction in pulmonary hypertension
Zhang B, Naik JS, Jernigan NL, Walker BR, Resta TC. Reduced membrane cholesterol limits pulmonary endothelial Ca2+ entry following chronic hypoxia. Am J Physiol 312(6):H1176-H1184, 2017.

Zhang B, Naik JS, Jernigan NL, Walker BR, Resta TC. Reduced membrane cholesterol following chronic hypoxia limits Orai1-mediated pulmonary endothelial Ca2+ entry. Am J Physiol. 314(2):H350-H369, 2018.