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Jianfeng Du

Researcher at Boston University

Publications -  14
Citations -  543

Jianfeng Du is an academic researcher from Boston University. The author has contributed to research in topics: Cardiac function curve & Ventricular remodeling. The author has an hindex of 10, co-authored 14 publications receiving 416 citations.

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Histone deacetylase (HDAC) inhibition improves myocardial function and prevents cardiac remodeling in diabetic mice

TL;DR: It is demonstrated that cardiac function was depressed in diabetic mice, but HDAC inhibition resulted in a significant functional improvement in STZ-injected mice, and myocardial superoxide dismutase, an important antioxidant, was elevated followingHDAC inhibition in the diabetic mice.
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Irisin plays a pivotal role to protect the heart against ischemia and reperfusion injury

TL;DR: Irisin serves as a novel approach to eliciting cardioprotection, which is associated with the improvement of mitochondrial function and significantly attenuated hypoxia/reoxygenation (H/R), as indicated by the reduction of lactate dehydrogenase (LDH) leakage and apoptotic cardiomyocytes.
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Sodium Butyrate Protects -Against High Fat Diet-Induced Cardiac Dysfunction and Metabolic Disorders in Type II Diabetic Mice.

TL;DR: It is suggested that HDAC inhibition plays a critical role to preserve cardiac performance and mitigate metabolic disorders in obesity and diabetes, which is associated with MKK3/p38/PRAK pathway.
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Stimulation of glucagon-like peptide-1 receptor through exendin-4 preserves myocardial performance and prevents cardiac remodeling in infarcted myocardium.

TL;DR: In this article, the authors demonstrated that GLP-1R with exendin-4 improved myocardial functional recovery in acute myocardious ischemic injury. But, they did not investigate whether GLP1R can improve the functional recovery.
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Specific inhibition of HDAC4 in cardiac progenitor cells enhances myocardial repairs.

TL;DR: Mouse myocardial infarction was created to assess the effect of HDAC4 inhibition in c-kit(+) CSCs on myocardIAL regeneration in vivo when cells were introduced into MI hearts, and results indicate that HDAC 4 inhibition promotes CSC-derived cardiac regeneration and improves the restoration of cardiac function.