Dr. Yong Zhou obtained his MD degree from Wuhan University, China and his PhD degree from Kyushu University, Japan.  He has been a recipient Yong Zhouof a Japanese Government Scholarship (also known as Monbusho Scholarship) from 1997 to 2002.  He completed his postdoctoral training at the Department of Pathology, UAB and was appointed Research Associate and then promoted to Instructor of Pathology.  In 2009, Dr. Zhou was appointed Assistant Professor of Medicine in the Division of Pulmonary, Allergy and Critical Care Medicine.  He is currently program committee member of American Thoracic Society Assembly on Respiratory Structure and Function and peer reviewer of the American Heart Association. 

Dr. Zhou’s research focuses on the mechanotransduction mechanisms by which cell and extracellular matrix (ECM)-derived mechanical stimuli regulate the pathogenesis of pulmonary fibrosis, particularly idiopathic pulmonary fibrosis (IPF).  Studies from his lab suggest that sustained myofibroblast contraction and matrix stiffening, characteristics of human IPF, provide feed-forward mechanisms for disease progression through both intrinsic and extrinsic mechanotransduction.  Recent collaborative work from his and Dr. Thannickal’s labs  demonstrates that blocking the mechanotransduction pathway selectively promotes fibrogenic effector cell death and ameliorates experimental pulmonary fibrosis in animal models.  In addition to  basic research in the area of mechanopathobiology, Dr. Zhou’s ongoing research involves bench-to-bedside translation of basic scien

DOM April 2013 paper of the month

J Clin Invest. 2013 Mar 1;123(3):1096-108. doi: 10.1172/JCI66700. Epub 2013 Feb 22.

Inhibition of mechanosensitive signaling in myofibroblasts ameliorates experimental pulmonary fibrosis.

Zhou Y, Huang X, Hecker L, Kurundkar D, Kurundkar A, Liu H, Jin TH, Desai L, Bernard K, Thannickal VJ.


Matrix stiffening and myofibroblast resistance to apoptosis are cardinal features of chronic fibrotic diseases involving diverse organ systems. The interactions between altered tissue biomechanics and cellular signaling that sustain progressive fibrosis are not well defined. In this study, we used ex vivo and in vivo approaches to define a mechanotransduction pathway involving Rho/Rho kinase (Rho/ROCK), actin cytoskeletal remodeling, and a mechanosensitive transcription factor, megakaryoblastic leukemia 1 (MKL1), that coordinately regulate myofibroblast differentiation and survival. Both in an experimental mouse model of lung fibrosis and in human subjects with idiopathic pulmonary fibrosis (IPF), we observed activation of the Rho/ROCK pathway, enhanced actin cytoskeletal polymerization, and MKL1 cytoplasmic-nuclear shuttling. Pharmacologic disruption of this mechanotransduction pathway with the ROCK inhibitor fasudil induced myofibroblast apoptosis through a mechanism involving downregulation of BCL-2 and activation of the intrinsic mitochondrial apoptotic pathway. Treatment with fasudil during the postinflammatory fibrotic phase of lung injury or genetic ablation of Mkl1 protected mice from experimental lung fibrosis. These studies indicate that targeting mechanosensitive signaling in myofibroblasts to trigger the intrinsic apoptosis pathway may be an effective approach for treatment of fibrotic disorders.

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