Assistant Professor in Medicine and of Molecular and Cellular Pathophysiology

Division of Pulmonary, Allergy & Critical Care Medicine
1530 3rd Avenue So, THT-422
University of Alabama at Birmingham
Birmingham, AL 35294


Campus Address:


 THT 422


Academic Office location:


 THT 437-B


Office Phone :


 (205) 975-2216


Office Fax:


 (205) 934-7121


Email Address:




Brief Bio

Dr. Zhou received his Bachelor in Medicine degree from Wuhan University, China in 1991 and his PhD degree from Kyushu University, Japan in 2002. He completed his Post-doctoral training at the University of Alabama at Birmingham. In 2007, Dr. Zhou joined the faculty at UAB and was appointed to the position of Instructor in the Department of Pathology. He later joined the Department of Medicine, in the Division of Pulmonary, Allergy and Critical Care Medicine as a tenure-earning Assistant Professor in 2009. Dr. Zhou has been a recipient of the Japanese Government Scholarship (Mobusho Scholarship) and is a recipient of the Young Investigator Award in the 15th International Colloquium on Lung and Airway Fibrosis 


Research Interests

Persistent myofibroblast differentiation is central to the pathogenesis of human idiopathic pulmonary fibrosis (IPF).  Myofibroblasts acquire contractile characteristics of smooth muscle cells and produce persistent isometric contractile forces by formation of alpha-smooth muscle actin-containing stress fibers. Recent advances suggest that mechanotransduction, a process through which cells convert mechanical stimuli into biochemical signals, plays a key role in regulating fibrotic phenotype in the lung. The stress fiber-generated forces are transmitted to the surrounding extracellular matrix (ECM) by transmembrane integrins. The force transmission results in a conformational change of the ECM-bound latent TGF-beta1 complex (termed as latent TGF-beta1 activation) that releases/exposes the C-terminal active TGF-beta1, a major profibrotic cytokine that is sufficient to promote myofibroblast differentiation. It is proposed that myofibroblast contraction-induced latent TGF-beta1 activation may be a driving-force for maintaining the persistent myofibroblastic phenotype observed in IPF lungs. We are interested in understanding the mechanisms involved in regulation of mechano-induced latent TGF-beta1 activation and lung myofibroblast differentiation. Our current work focuses on identifying potential factors that regulate myofibroblast contractility and differentiation. The goals are to provide further mechanistic insights into the role of mechanotransduction in the pathogenesis of IPF and to develop effective therapeutic interventions for IPF treatment with a new approach.

Emphysema is a chronic obstructive lung disease characterized by the damage of elastin fibers. Repair of the damaged elastic fibers requires coordinated actions of both the molecules that make up the microfibrils and the helper proteins to facilitate elastic fiber assembly. Latent TGF-beta binding protein (LTBP)-4 is a lately identified member of fibrillin/LTBP family in which many members are known as the regulators of TGF-beta bioavailability and activation. LTBP-4 interacts with fibrillins and is an essential component of the sheath of microfibrils that surround the elastin core of elastin fibers. Mice deficient in LTBP-4 develop emphysema-like lung morphology. Perturbation of TGF-beta function has been shown in association with emphysema development. We have recently demonstrated that LTBP-4 is essential for latent TGF-beta1 activation by lung fibroblasts in response to lung injury. Another research area in the lab is to determine the role of LTBP-4 in elastic fiber repair.

 Dr. Zhou's Lab is currently funded by the NIH and the  American Heart Association.


 Key Publications

Zhou Y, Koli K, Hagood JS, Miao M, Mavalli M, Rifkin DB and Murphy-Ullrich JE. Latent TGF-beta binding protein (LTBP)-4 regulates TGF-beta1 bioavailability for activation by fibrogenic lung fibroblasts in response to bleomycin. Am J Pathology. 2009 Jan;174(1):21-33. 

Zhou Y, Hagood JS, Murphy-Ullrich JE. Thy-1 expression regulates the ability of rat lung fibroblasts to activate TGF-beta in response to fibrogenic stimuli. Am J Pathology. 2004 Aug;165(2):659-69

Zhou Y*, Hagood JS, Lu B, Merryman WD, Murphy-Ullrich JE. Thy-1-integrin alphavbeta5 interactions inhibit lung fibroblast contraction-induced latent transforming growth factor-beta1 activation and myofibroblast differentiation. J Biol Chem. 2010 Jul;285(29):22382-93 *Corresponding author

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