Dr. Hongwei Yao is appointed as an Associate Professor of Molecular Biology, Cellular Biology & Biochemistry (Research) at Brown University Warren Alpert Medical School after his postdoctoral training and first faculty appointment as an Assistant Professor (Research) in the Department of Environmental Medicine of the University of Rochester. His research focuses on molecular pathogenesis and potential therapeutic targets in chronic lung diseases including adult Chronic Obstructive Pulmonary Disease (COPD) and pulmonary fibrosis as well as neonatal Bronchopulmonary Dysplasia (BPD) using in vitro in cells, in vivo in animals and ex vivo in human peripheral tissues. Dr. Yao has approximate 15 years’ experience and expertise in lung oxidative stress, inflammation, cellular senescence, metabolism, and mitochondrial autophagy (mitophagy).
Dr. Yao has a strong and track record of first/corresponding author articles in high impact journals (e.g., Br J Pharmcol 2016, FASEB J 2015, J Clin Invest 2012, Proc Natl Acad Sci USA 2010, J Biol Chem 2010) with total >100 co-author publications including original article, reviews, and book chapters. The total citations for these publications are >3,000 with H-index of 31 till July 2018. Due to scientific contributions, Dr. Yao won several awards and has been frequently invited to present his work at local, national and international forums and conferences.
Dr. Yao has been serving as an Ad-hoc member of several panels of federal grant study sections including the NIH. Dr. Yao was/is a member of the editorial board of several international journals, such as American Journal of Physiology-Lung Cellular and Molecular Physiology. He also serves as a reviewer for more than 50 peer-reviewed journals including American Journal of Respiratory and Critical Care Medicine.
Dr. Yao’s research has been supported by the National Natural Science Foundation of China and American Lung Association as well as CardioPulmonary Vascular Biology COBRE Pilot Project as a PI. Dr. Yao’s work, as the Project 1 of the Phase II CPVB/COBRE, focuses on whether metabolic dysregulation contributes to lung endothelial cell dysfunction implicating arrested angiogenesis during hyperoxic lung injury. This would lead to a potential conceptual shift regarding metabolic reprogramming in the pathogenesis of BPD, where premature infants with BPD usually need supplemental oxygen for therapy.
Bronchopulmonary dysplasia (BPD) is a chronic lung disease, which is characterized by alveolar dysplasia and impaired vascularization. BPD is defined clinically by continued dependency on supplemental oxygen beyond 36 weeks corrected gestation in premature infants. Although most BPD survivors eventually can be weaned from supplemental oxygen, there can be residual pulmonary dysfunction and cardiovascular sequelae in adolescence and adulthood. However, oxygen supplementation can disrupt normal lung development and blunt the growth of pulmonary microvasculature (vessel sprouting). Blood vessel growth is tightly linked to metabolic status in endothelial cells (ECs); with both glycolysis and mitochondrial fatty acid oxidation (FAO) being essential for EC proliferation and vessel sprouting. It is not known, however, whether hyperoxic exposure alters lung EC metabolism leading to impaired vascularization, alveolar dysplasia, and subsequent lung injury. We hypothesize that hyperoxic exposure causes FA accumulation, whereas enhancing FAO protects against hyperoxia-induced lung EC apoptosis and subsequent impaired vascularization and alveolarization in neonates. Therefore, we propose to determine: 1) the mechanisms underlying hyperoxia-induced initial increases in FAO in lung ECs; 2) how FAO modulates lung EC apoptosis in response to hyperoxic exposure; 3) the role of FAO in hyperoxia-induced impaired vascularization and alveolarization in neonatal mice. The work will uncover novel metabolic mechanisms for hyperoxia-induced impairment of pulmonary vascularization and alveolarization. In turn, this will have a significant translational potential in the development of pharmacological and molecular approaches targeting fatty acid catabolism to ameliorate lung injury and cardiovascular sequelae in BPD.
He is the Principle Investigator of Project 1 from the Phase II CPVB/COBRE entitled, “Metabolic mechanisms of impaired vascularization during hyperoxic lung injury.”
Phyllis Dennery, MD
Professor of Pediatrics, Professor of Molecular Biology, Cell Biology and Biochemistry, Chair of Pediatrics, Brown University
Brown University Research UTRA Award (Mentor)
American Lung Association (PI)
National Natural Science Foundation of China (PI)
Ocean State Research Institute
Providence VA Medical Center
830 Chalkstone Avenue
Providence RI 02908
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Research reported in this website was supported by the National Institute of General Medical Science of the National Institutes of Health under grant number P20GM103652.