ATP2B1 Gene Silencing Increases NO Production Under Basal Conditions Through the Ca2+/calmodulin/eNOS Signaling Pathway in Endothelial Cells-Reference-Cited by-同舟云学术

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ATP2B1 Gene Silencing Increases NO Production Under Basal Conditions Through the Ca2+/calmodulin/eNOS Signaling Pathway in Endothelial Cells

Published:2018-02-07 Issue:4 Volume:41 Page:246-252
ISSN:0916-9636
Container-title:Hypertension Research
language:en
Short-container-title:Hypertens Res

Author:

Long Yang,Chen Shao-wei,Gao Chen-lin,He Xue-mei,Liang Guan-nan,Wu Jian,Jiang Chun-xia,Liu Xin,Wang Fang,Chen Feng

Publisher

Springer Science and Business Media LLC

Subject

Cardiology and Cardiovascular Medicine,Physiology,Internal Medicine

Link

http://www.nature.com/articles/s41440-018-0012-x.pdf

Reference25 articles.

1. WHO. Global status report on noncommunicable disease 2014; 2014.

2. NCD-RisC. Worldwide trends in blood pressure from 1975 to 2015: a pooled analysis of 1479 population-based measurement studies with 19.1 million participants. Lancet . 2017;389:37–55.

3. WHO. Global health risks: Mortality and burden of disease attributable to selected major risks; 2009.

4. Li Q, Youn JY, Cai H. Mechanisms and consequences of endothelial nitric oxide synthase dysfunction in hypertension. J Hypertens. 2015;33:1128–36.

5. Joannides R, Haefeli WE, Linder L, Richard V, Bakkali EH, Thuillez C, Luscher TF. Nitric oxide is responsible for flow-dependent dilatation of human peripheral conduit arteries in vivo. Circulation . 1995;91:1314–9.

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