people

Department Directory

Faculty

Faculty by areas of interest

Emeritus Faculty

Students

Postdocs

Staff

Alumni

Former Postdocs

 

Student Profiles

Alumni Profiles

Faculty Essays

 

 

PBIO Photo Gallery

Facultyfaculty photo


Qinghang (Chris) Liu
Assistant Professor
Ph.D. Physiology, University of Tennessee Health Science Center, 2004
Office phone: (206) 685-9133
qcliu@uw.edu

 

MOLECULAR SIGNALING MECHANISMS OF CARDIAC HYPERTROPHY AND HEART FAILURE

Hypertrophic heart disease and heart failure are the major causes of morbidity and mortality in the United States and other developed countries. For adult cardiac muscle, the single most common target of disease in the elderly, the characteristic response to pathological stress (e.g., hypertension, myocardial infarction, and inherited cardiomyopathy) is cardiac muscle enlargement, termed cardiac hypertrophy. Cardiac hypertrophy is initially a compensatory process that attempts to maintain or augment pump function, however, prolongation of this process leads to congestive heart failure, arrhythmia, and sudden death. Cardiac hypertrophy is associated with transcriptional reprogramming, pathological remodeling, and progression to heart failure, with ventricular wall thinning, chamber dilation, and myocyte death.

A better characterization of the signaling networks that control hypertrophy-specific gene expression will be paramount for designing novel therapeutic approaches with translational potential for heart failure. My research is focused on defining novel molecular signaling mechanisms regulating cell growth and survival during physiological conditions and during cardiac hypertrophy and heart failure. We use genetically altered mice as model systems. We also use viral vector mediated gene transfer in cultured cardiomyocytes and other cell systems to investigate molecular signaling mechanisms underlying the cardiomyocyte hypertrophic growth and cell death.

We are particularly interested in elucidating novel cell signaling mechanisms in the heart involving protein kinases (e.g, PKC, ASK1, and TAK1) and phosphatases (e.g, PP1, PP2A, and calcineurin). Currently we are evaluating the role of TGFβ activated Kinase 1 (TAK1) as a central regulator of the hypertrophic signaling network in vivo using cardiac specific TAK1 transgenic and gene targeted mouse models. Our approach may suggest novel therapeutic strategies for the treatment of heart failure if conclusive proof is established in animal models. The laboratory is also interested in defining transcriptional regulatory mechanisms of cardiomyocyte growth and survival, with a focus on transcription factors NFAT and NFkB. Understanding of regulatory mechanisms of target gene expression will shed additional light on the regulatory paradigms that underlie cardiac hypertrophy and heart failure.