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The research in our lab primarily focuses on the contribution of the extracellular matrix (ECM) and its interaction with the resident cells, in cardiac and vascular pathologies.  Physiological turnover of the ECM is mediated by matrix metalloproteinases (MMPs) that degrade the existing proteins to be replaced with new proteins, while their activity is kept under control by the inhibitory function of TIMPs (Tissue Inhibitor of Metalloproteinases). TIMPs are a family of 4 members (TIMPs1-4) that collectively inhibit almost all 24 members of the MMP family. In addition to MMPs, some TIMPs can inhibit other proteases such as ADAMs (a disintegrin and metalloproteinases) and ADAM-TSs (ADAM with Thrombospondin motifs) that regulate various cellular events. Reports from our lab and other laboratories have revealed that the ECM does not only provide a structural support for the heart and the vascular tissue (as well as in other organs), but it is a microenvironment for storage of a numerous growth factors and cytokines.

Our lab has been interested in exploring the novel aspects of ECM function in cardiovascular pathologies, for instance, the role of non-fibrillar ECM proteins, novel functions of TIMPs and MMPs, and the contribution of non-MMP proteases in cardiovascular pathologies. 


Research Approaches and Models


Our research takes a comprehensive approach which covers the full spectrum of events from molecular and in vitro cellular events to ex vivo organ function and in vivo disease models. We utilize genetically modified mice (knock out, cell specific knockout, and inducible cell-specific Knockout), and animal models of common human cardiovascular diseases such as myocardial infarction/heart attack (by LAD ligation), ischemia-reperfusion (in vivo: temporary LAD ligation), cardiac pressure overload (aortic constriction), hypertrophic and dilated cardiomyopathies, hypertension (Ang II infusion), thoracic and abdominal aortic aneurysm (periadventitial elastase exposure; Ang II infusion in genetically predisposed mice), and atherosclerosis (Ldlr-deficiency + atherogenic diet). Importantly, our access to human heart and aorta specimens has given us the unique opportunity to validate our animal models in human tissue and human cells.  

We utilize in vitro culture systems of cardiomyocyes, fibroblasts, vascular smooth muscle cells and endothelial cells (mouse and human) to explore the mechanism of action for the molecules of interest (e.g. TIMPs, MMPs, ADAMs, etc) and to dissect the cell-cell interactions.

Myocardial infarction (MI) and postischemia/reperfusion (I/R) injury

MI and I/R Injury

Pressure overload or agonist-induced hypertension and cardiac hypertrophy

Cardiac Hypertrophy and Hypertension

Thoracic aortic aneurysm (TAA) and abdominal aortic aneurysm (AAA)

Aortic Aneurysm

Lipid metabolism and  atherosclerosis

Lipid Metabolism and Atherosclerosis

Loss of TIMP4 increased plaque accumulation in the abdominal aorta despite lower

plasma cholesterol level.

Hu et al. Artheriosclerosis,Thromb. & Vasc. Biol. (ATVB) 2021 


We are extremely grateful to the following agencies for funding our research

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