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Q

Qiang Wang

Researcher at Nanjing University

Publications -  24
Citations -  2603

Qiang Wang is an academic researcher from Nanjing University. The author has contributed to research in topics: Median sternotomy & Endothelial stem cell. The author has an hindex of 9, co-authored 18 publications receiving 2340 citations.

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Secreted Monocytic miR-150 Enhances Targeted Endothelial Cell Migration

TL;DR: It is reported that secreted miRNAs can serve as signaling molecules mediating intercellular communication and demonstrate that cells can secrete miRNA and deliver them into recipient cells where the exogenous mi RNAs can regulate target gene expression and recipient cell function.
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Exogenous plant MIR168a specifically targets mammalian LDLRAP1: Evidence of cross-kingdom regulation by microRNA

TL;DR: It is shown that MIR168a could bind to the human/mouse low-density lipoprotein receptor adapter protein 1 (LDLRAP1) mRNA, inhibit LDLRAP1 expression in liver, and consequently decrease LDL removal from mouse plasma, demonstrating that exogenous plant miRNAs in food can regulate the expression of target genes in mammals.
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Microvesicle-mediated Transfer of MicroRNA-150 from Monocytes to Endothelial Cells Promotes Angiogenesis

TL;DR: It is demonstrated that secretion of miR-150 via MVs can promote angiogenesis in vitro and in vivo, and a novel microRNA-based therapeutic approach for disease treatment is presented.
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MicroRNA-19b/221/222 induces endothelial cell dysfunction via suppression of PGC-1α in the progression of atherosclerosis

TL;DR: The posttranscriptional regulation of PGC-1α by miR-19b/221/222 was unveiled, which provides a novel mechanism in which a panel of microRNAs can modulate endothelial cell apoptosis via the regulation mitochondrial function.
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Hypoxia induces PGC-1α expression and mitochondrial biogenesis in the myocardium of TOF patients.

TL;DR: It is shown that hypoxia can stimulate the expression of PGC-1α and mitochondrial biogenesis in the cardiac myocytes, and this process might provide a potential adaptive mechanism for cardiac myocyte to increase ATP output and minimize hypoxic damage to the heart.