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Jian Yang

Researcher at Chongqing Medical University

Publications -  59
Citations -  1070

Jian Yang is an academic researcher from Chongqing Medical University. The author has contributed to research in topics: Receptor & Kidney. The author has an hindex of 15, co-authored 52 publications receiving 741 citations. Previous affiliations of Jian Yang include University of Maryland, Baltimore & National Institutes of Health.

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Mesenchymal stem cells-derived extracellular vesicles, via miR-210, improve infarcted cardiac function by promotion of angiogenesis.

TL;DR: MSC-EVs are sufficient to improve angiogenesis and exert therapeutic effect on MI, its pro-angiogenesis effect might be associated with a miR-210-Efna3 dependent mechanism.
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EGCG attenuates high glucose-induced endothelial cell inflammation by suppression of PKC and NF-κB signaling in human umbilical vein endothelial cells.

TL;DR: EGCG suppresses high glucose-induced vascular inflammatory process via the inhibition of PKC and NF-κB activation in HUVECs, suggesting that EGCG may be a potential candidate for the treatment and prevention of diabetic vascular complications.
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Angiotensin II AT2 receptor decreases AT1 receptor expression and function via nitric oxide/cGMP/Sp1 in renal proximal tubule cells from Wistar–Kyoto rats

TL;DR: The results indicate that the renal AT2 receptor, via nitric oxide/cGMP/Sp1 pathway, regulates AT1 receptor expression and function, which may be important in the regulation of sodium excretion and blood pressure.
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Curcumin Exerts its Anti-hypertensive Effect by Down-regulating the AT1 Receptor in Vascular Smooth Muscle Cells.

TL;DR: Findings indicate that curcumin down-regulates AT1R expression in A10 cells by affecting SP1/AT1R DNA binding, thus reducing At1R-mediated vasoconstriction and subsequently prevents the development of hypertension in an Ang II-induced hypertensive model.
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Pro-atherogenic role of smooth muscle Nox4-based NADPH oxidase

TL;DR: Gene analysis indicated that soluble epoxide hydrolase 2 (sEH) was significantly downregulated in Nox4DN smooth muscle cells (SMC), at both mRNA and protein levels, which accounts for inhibition of SMC proliferation, migration and inflammation.