Dr. Zhou obtained his MD degree from Wuhan University in China and his PhD from Kyshu University in Japan. He completed his postdoctoral studies in the area of TGF-beta, matrix biology, and lung fibrosis at the University of Alabama at Birmingham, where he later became a Department of Pathology faculty member. In 2009, Dr. Zhou was recruited to the Department of Medicine, Division of Pulmonary, Allergy, and Critical Care Medicine, where he is now an Associate Professor of Medicine. Dr. Zhou has recieved many prestigious awards, including the International Colloquium on Lung and Airway Fibrosis (ICLAF) Young Investigator Award, the American Thorasic Society (ATS) Recognition Award for Outstanding Early Career Investigator, and the UAB School of Medicine Dean's Excellence Award in Mentoring.
Dr. Zhou currently serves as a PLOS ONE editorial board member, a grant reviewer for the American Heart Association (AHA), and a grant reviewer for the Department of Defense (DoD). He has served on ATS International Conferences as chair, co-chair, and facilitator and has also served on the program committee of the ATS Assembly on Respiratory Structure and Function (RSF).
Dr. Zhou conducts basic scientific research in the area of pulmonary and ocular mechanobiology.
Pulmonary fibrosis is characterized by substantional changes in the mechanical properties of the lung. One promient change is stiffenting of the extracellular matrix (ECM). Research in Dr. Zhou's laboratory aims to understand how stiffened fibrotic matrix-derived mechanical signals are sensed by lung cells (fibroblasts, alveolar epithelial cells, and macrophages), how they are further converted into biochemical signals within the cells, and how the mechanotransduction may regulate changes in cell phenotype that feed back into the ongoing lung injury-repair process. The goal of this research is to identify key mediators in the mechanotransduction pathways and to develop novel theraputic agents to target the deleterious biomechanical signaling for treating persistent/progressive lung fibrosis.
Dr. Zhou's lab also works to deteming cellular responses to intraocular pressure-generated mechanical strain that drive ECM remodeling in lamina cribosa cells and scleral fibroblasts harvested from clinical-records-confirmed normal and glaucomatous human donor eyes. Progressive remodeling of load-bearing connective tissues, like lamina cribosa and sclera, at the optic nerv head, is a defining feature of glaucoma. This remodeling alters the microenvironment of the retinal ganglion cell (RGC) axons traversing the ONH and is believed to be a direct cause of the axon loss and death of RGCs. Intraocular pressure is currently the only known modifiable risk factor for glaucoma.
Dr. Zhou's Lab is currently funded by the NIH/NHLBI, AHA, ATS, and the EyeSight Foundation of Alabama (ESFA).
Zhou Y, Chen H, Ambalavanan N, Liu G, Antony VB, Ding Q, Nath H, Eary J and Thannickal VJ. Noninvasive Imaging of Experimental Lung Fibrosis. Am J Respir Cell Mol Biol. 2015 2015 Jul;53(1):8-13.
Li H, Fu Y-X, Wu Q, Zhou Y, Crossman DK, Yang P, Li J, Luo B, Morel LM, Kabarowski JH, Yagita H, Ware C, Hsu H-C, and Mountz JD. Type I Interferons Promote Lupus via Disruption of the Lymphotoxin Receptor-mediated Mechanosensing MKL1 Pathway in the Spleen Marginal Zone Macrophages. J Clin Invest. 2015 Jul 1;125(7):2877-90.
Thannickal VJ, Zhou Y, Gaggar A and Duncan SR. Fibrosis: Proximate and Ultimate Causes. J Clin Invest. 2014 Nov 3;124(11):4673-7.
Zhou Y, Huang X, Hecker L, Kurundkar D, Kurundkar A, Liu H, Jin T-H, Desai L, Bernard K, and Thannickal VJ. Inhibition of mechanosensitive signaling in myofibroblasts ameliorates experimental pulmonary fibrosis. J Clin Invest. 2013 123(3):1096-108
Huang X, Yang N, Fiore VF, Barker TH, Sun Y, Morris SW, Ding Q, Thannickal VJ, Zhou Y. Matrix stiffness-induced myofibroblast differentiation is mediated by intrinsic mechanotransduction. Am J Respir Cell Mol Biol. 2012 Sep;47(3):340-8.
Please click here for Dr. Zhou's complete publication listing.