Research in Dr. Chen’s laboratory focuses on investigating the mechanisms of cardiac diseases and identifying the appropriate pharmacological agents being able to recover cardiac function. We use a variety of approaches, including electrophysiology, imaging, molecular biology, genetics, and proteomics, to understand the problems and design solutions in the laboratory and then demonstrate the effectiveness of these solutions in vivo. We use myocardial infarction animal model to assess drug effect in preventing the heart from lethal arrhythmia and failure, and aortic banding animal model to identify drugs against cardiac remodeling.

More recently, the cardiomyocytes renewal in human was reported that fewer than 50% of cardiomyocytes are exchanged during a normal life span. By using lineage-tracing method, a population of Nkx2.5-eGFP⁺ precursor cells can be isolated from the postnatal Nkx2.5-eGFP transgenic mice. It might be a promising cardiac regenerative strategy via expanding the residual cardiac precursors to compensate the loss of cardiomyocytes in heart diseases. Accordingly, one of my current projects is focusing on the pharmacological mechanisms in regulating the expansion and differentiation of cardiac Nkx2.5-GFP⁺ precursors, and assessing whether Nkx2.5⁺ cell expansion can prevent the heart from cardiac remodeling and heart failure. We are also interested in the durability and functional properties of the regenerated cardiac cells.

近期代表著作：

1] Small molecule regulators of postnatal Nkx2.5 cardiomyoblast proliferation and differentiation. J Cell Mol Med. 16(5):961-5.  2012.  [Abstract]

2] Intracellular zinc release-activated ERK-dependent GSK-3beta-p53 and Noxa-Mcl-1 signaling are both involved in cardiac ischemic-reperfusion injury. Cell Death Differ,18:1651-1663. 2011. [Abstract]

3] Thaliporphine ameliorates cardiac depression in endotoxemic rats through attenuating TLR4 signaling in the downstream of TAK-1 phosphorylation and NF-κB signaling. Naunyn Schmiedeberg's archives of pharmacology,382:441-453. 2010. [Abstract]

4] Piceatannol, a derivative of resveratrol, moderately slows I(Na) inactivation and exerts antiarrhythmic action in ischaemia-reperfused rat hearts. Br J Pharmacol,157:381-391. 2009. [Abstract]

5] Serine-385 phosphorylation of inwardly rectifying k+ channel subunit (kir6.2) by amp-dependent protein kinase plays a key role in rosiglitazone-induced closure of the k(atp) channel and insulin secretion in rats. Diabetologia,52:1112-1121. 2009.  [Abstract]

1]   Regulating cardiac precursors expansion and differentiation

2]  Cardiac remodeling

3]  Diabetic cardiomyopathy

4]  Antiarrhythmic agents