Hongwei Yao, PhD

Associate Professor (Research)
Department of Molecular Biology, Cell Biology & Biochemistry
Brown University Warren Alpert Medical School

Tel: 401-863-6754
Fax: 401-863-1201
E-mail: Hongwei_Yao@brown.edu

Hongwei Yao, PhD


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, 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 >2,100 with H-index of 27 till July 2016. 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 a member of several panels of federal grant study section as an Ad-hoc, such as National Natural Science Foundation of China, British Lung Foundation, and Florida DOH funding agencies. Dr. Yao is a member of the editorial board of several international journals, such as Journal of Respiratory Research and Frontiers in Respiratory Pharmacology. He also serves as an Ad hoc reviewer for more than 50 peer-reviewed journals including American Journal of Respiratory Cell and Molecular Biology and Scientific Reports.

Dr. Yao’s research has been supported by the National Natural Science Foundation of China and American Lung Association as a PI. Recently, Dr. Yao’s work was awarded by the CardioPulmonary Vascular Biology COBRE Pilot Project (2016-2017), which 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.

COBRE Abstract

Although premature infants can survive at extremes of gestation (> 22 weeks), the treatments with mechanical ventilation and supplemental oxygen disrupt normal lung development and blunt the growth of pulmonary microvasculature (vessel sprouting) and distal airspaces. This results in continued dependency on supplemental oxygen beyond 36 weeks corrected gestation, referred to as bronchopulmonary dysplasia (BPD). The lung pathology of BPD can be mimicked in rodents exposed to hyperoxia as neonates. Hyperoxic exposure reduces mitochondrial respiration in lung cells, but its effect on mitochondrial utilization of fuels (i.e., glucose, fatty acid, and glutamine) particularly in endothelial cells remains unknown. Endothelial cells primarily rely on glycolysis for bioenergetics. Under oxidative stress, endothelial cells can switch glycolytic flux to the pentose phosphate pathway (PPP) so as to generate the reducing equivalent NADPH. The inhibition of glycolysis reduces vessel sprouting. However, it is not known whether hyperoxia alters mitochondrial fuel utilization or results in the PPP switch, leading to pulmonary endothelial dysfunction and disrupted angiogenesis during the development of BPD. We hypothesize that hyperoxic exposure disrupts metabolic homeostasis leading to pulmonary endothelial dysfunction. To test this hypothesis, we propose the following two Specific Aims to determine: 1) the changes in mitochondrial fuel utilization in lung endothelial cells exposed to hyperoxia; 2) roles of glycolysis vs. PPP in hyperoxia-induced lung endothelial cell dysfunction. The outcome of this proposal will not only identify the metabolic switch during hyperoxic exposure, but also unravel the role of glycolysis vs PPP in hyperoxia-induced pulmonary endothelial dysfunction. In turn, this will provide an understanding of mechanisms underlying hyperoxia-induced arrest of pulmonary vascularization, and will also provide the rationale for designing therapeutic strategies to ameliorate dysregulated metabolism and lung injury in the prevention of BPD.

Project Updates

He is the Principle Investigator of a 5-month pilot project form the CPVB COBRE entitled, “Metabolic Dysregulation in Pulmonary Endothelial Dysfunction during Hyperoxic Lung Injury.”



Mentors and their website links:
Dr. Phyllis Dennery: https://vivo.brown.edu/display/pdennery

Dr. Sharon Rounds: https://vivo.brown.edu/display/srounds