2026-05-17T01:43:54Zhttps://repisalud.isciii.es/rest/oai/requestoai:repisalud.isciii.es:20.500.12105/79162024-09-27T08:59:36Zcom_20.500.12105_19604com_20.500.12105_2051col_20.500.12105_19605
Repisalud
author
Andres, Vicente
funder
Ministerio de Economía y Competitividad (España)
funder
Instituto de Salud Carlos III
funder
Unión Europea. Fondo Europeo de Desarrollo Regional (FEDER/ERDF)
funder
Unión Europea. Comisión Europea
funder
Progeria Research Foundation
funder
Fundación ProCNIC
2019-07-17T06:16:34Z
2019-07-17T06:16:34Z
2014-10
Atherosclerosis. 2014; 236(2):444-447
10.1016/j.atherosclerosis.2014.07.031
1879-1484
0021-9150
Atherosclerosis
25173069
http://hdl.handle.net/20.500.12105/7916
Signaling via both vitamin D (VitD) and the renin-angiotensin system (RAS) plays important roles in physiological processes. Evidence has mounted linking cardiovascular disease to both increased activity of the RAS and VitD deficiency. Although several studies have established functional relationships between the RAS and VitD, many aspects of their complex interaction remain unknown. In this issue of Atherosclerosis, Valcheva and colleagues show that defective VitD signaling can promote vascular damage by inducing premature senescence of smooth muscle cells due to elevated local production of angiotensin II and reactive oxygen species, and upregulation of the tumor suppressor p57(Kip2).
eng
Angiotensin
Cell senescence
Vascular smooth muscle cell
Vitamin D
p57
Vitamin D puts the brakes on angiotensin II-induced oxidative stress and vascular smooth muscle cell senescence
journal article
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URL
https://repisalud.isciii.es/bitstreams/1ea2c2d6-40c7-4966-aec5-7d0baafdc916/download
File
MD5
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application/pdf
VitaminDPutsBrakes_2014.pdf
URL
https://repisalud.isciii.es/bitstreams/23d7690a-6e91-42f4-9894-ada196b8042c/download
File
MD5
97aa0869d55160d45ba561dc8de8efcd
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text/plain
VitaminDPutsBrakes_2014.pdf.txt