Yiu-Fai Chen, PhD, FAHA

Chen-YiuFaiAssistant Professor

Dept. of Medicine
Division of Cardiovascular Diseases

Contact Information:

Office Address: Zeigler 1008
Phone: 205-934-1697
E-mail: This email address is being protected from spambots. You need JavaScript enabled to view it.
Websites: School of Medicine Faculty Profile

Education:

National Taiwan University, Taipei, Taiwan
BS, Zoology, 1975

National Taiwan University, Taipei, Taiwan
MS, Zoology, 1977

University of Illinois, Champaign-Urbana
MS, Physiology & Biophysics, 1979

University of Illinois, Champaign-Urbana
PhD, Physiology & Biophysics, 1982

Post-Graduate Training:

University of Alabama at Birmingham
Postdoctoral Fellow, Cardiovascular Research & Training Center, 1982-5

University of California at San Diego
NIH Senior Fellow, Bugher Foundation Center for Molecular Biology, 1991-2

Research Description:

The overall goal of our laboratory is to investigate the protective role of atrial natriuretic peptide (ANP) in pressure overload-induced cardiac hypertrophy/remodeling/fibrosis and in hypoxia-induced pulmonary hypertension and vascular remodeling.  Our major areas of interest are: 1) testing the hypothesis that during pressure overload stress, expression of both anti-fibrogenic factor ANP and pro-fibrogenic/growth factors (e.g. transforming growth factor [TGF]-β and angiotensin II [ANGII]) is enhanced in heart; the pro-fibrogenic/growth factors contribute to cardiac remodeling with increased cardiac fibrosis and eventual cardiac dysfunction, while the increased ANP plays a counter regulatory role and protects against these events; 2) investigating the intracellular signaling mechanisms leading to pro-fibrogenic/growth factor-stimulated cardiac fibroblast proliferation/transformation and extracellular matrix (ECM) molecule expression, and testing the hypothesis that anti-fibrogenic ANP-cGMP-protein kinase G (PKG) signaling inhibits, and pro-fibrogenic factor (e.g. TGF-b or ANGII)  signaling stimulates these processes; 3) testing the hypotheses that during hypoxic exposure, ANP acts an anti-fibrogenic factor to regulate ECM production in lung, and that without the counter regulatory/inhibitory effects of the ANP-cGMP-PKG signaling pathway, animals will develop exaggerated pulmonary arterial smooth muscle cell (PASMC) growth and proliferation, increased ECM deposition in lung, and more severe pulmonary hypertension, pulmonary vascular remodeling and fibrosis with hypoxic exposure; 4) investigating the intracellular signaling mechanisms leading to hypoxia- and pro-fibrogenic/growth factor-stimulated PASMC proliferation/growth and ECM expression. 

Projects currently underway in our laboratory include studies involving transgenic mouse models and isolated cardiac fibroblasts and PASMCs.  We use a range of state-of-the-art physiological, morphometric, biochemical and molecular techniques in the in vivo and in vitro studies.   We are also currently exploring gene microarray, proteomic and laser capture methods for the identification and characterization of gene and proteins that may play important roles in the remodeling/fibrosis of heart and lung under stressful conditions.

Publications

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