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Chunxiang Zhang

Researcher at Rush University Medical Center

Publications -  56
Citations -  6913

Chunxiang Zhang is an academic researcher from Rush University Medical Center. The author has contributed to research in topics: Vascular smooth muscle & microRNA. The author has an hindex of 32, co-authored 56 publications receiving 6449 citations. Previous affiliations of Chunxiang Zhang include University of Tennessee Health Science Center & Rutgers University.

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MicroRNA Expression Signature and Antisense-Mediated Depletion Reveal an Essential Role of MicroRNA in Vascular Neointimal Lesion Formation

TL;DR: The results suggest that miRNAs are novel regulatory RNAs for neointimal lesion formation and may be a new therapeutic target for proliferative vascular diseases such as atherosclerosis, postangioplasty restenosis, transplantation arteriopathy, and stroke.
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MicroRNA-145, a novel smooth muscle cell phenotypic marker and modulator, controls vascular neointimal lesion formation.

TL;DR: It is demonstrated that miR-145 is a novel VSMC phenotypic marker and modulator that is able of controlling vascular neointimal lesion formation and this finding may have extensive implications for the diagnosis and therapy of a variety of proliferative vascular diseases.
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MicroRNAs Are Aberrantly Expressed in Hypertrophic Heart : Do They Play a Role in Cardiac Hypertrophy?

TL;DR: It is demonstrated that miRNAs are aberrantly expressed in hypertrophic mouse hearts, and modulating miR-21 expression via antisense-mediated depletion (knockdown) had a significant negative effect on cardiomyocyte hypertrophy.
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A Necessary Role of miR-221 and miR-222 in Vascular Smooth Muscle Cell Proliferation and Neointimal Hyperplasia

TL;DR: MiR-221 and miR-222 are novel regulators for VSMC proliferation and neointimal hyperplasia and may also represent promising therapeutic targets in proliferative vascular diseases.
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MicroRNA Expression Signature and the Role of MicroRNA-21 in the Early Phase of Acute Myocardial Infarction

TL;DR: It is identified that miR-21 had a protective effect on ischemia-induced cell apoptosis that was associated with its target gene programmed cell death 4 and activator protein 1 pathway and was further confirmed in vivo by decreasedcell apoptosis in the border and infarcted areas of the infarCTed rat hearts after treatment with Ad-miR- 21.