Circulating miR-103a-3p contributes to angiotensin II-induced renal inflammation and fibrosis via a SNRK/NF-κB/p65 regulatory axis

Angiotensin II is known to cause renal inflammation and fibrosis. Here Lu et al. show that levels of circulating miR-103a-3p are elevated in hypertensive nephropathy patients and in an animal model of angiotensin II-induced renal dysfunction, and that miR-103a-3p suppresses SNRK expression leading t...

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Autores principales:	Qiulun Lu, Zejun Ma, Ye Ding, Tatiana Bedarida, Liming Chen, Zhonglin Xie, Ping Song, Ming-Hui Zou
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2019
Materias:	Science Q
Acceso en línea:	https://doaj.org/article/fb3cafbacbca473e82a1356b6b780951
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id	oai:doaj.org-article:fb3cafbacbca473e82a1356b6b780951
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spelling	oai:doaj.org-article:fb3cafbacbca473e82a1356b6b7809512021-12-02T15:35:11ZCirculating miR-103a-3p contributes to angiotensin II-induced renal inflammation and fibrosis via a SNRK/NF-κB/p65 regulatory axis10.1038/s41467-019-10116-02041-1723https://doaj.org/article/fb3cafbacbca473e82a1356b6b7809512019-05-01T00:00:00Zhttps://doi.org/10.1038/s41467-019-10116-0https://doaj.org/toc/2041-1723Angiotensin II is known to cause renal inflammation and fibrosis. Here Lu et al. show that levels of circulating miR-103a-3p are elevated in hypertensive nephropathy patients and in an animal model of angiotensin II-induced renal dysfunction, and that miR-103a-3p suppresses SNRK expression leading to the activation of the pro-inflammatory NF-κB pathway in glomerular endothelial cells.Qiulun LuZejun MaYe DingTatiana BedaridaLiming ChenZhonglin XiePing SongMing-Hui ZouNature PortfolioarticleScienceQENNature Communications, Vol 10, Iss 1, Pp 1-14 (2019)
institution	DOAJ
collection	DOAJ
language	EN
topic	Science Q
spellingShingle	Science Q Qiulun Lu Zejun Ma Ye Ding Tatiana Bedarida Liming Chen Zhonglin Xie Ping Song Ming-Hui Zou Circulating miR-103a-3p contributes to angiotensin II-induced renal inflammation and fibrosis via a SNRK/NF-κB/p65 regulatory axis
description	Angiotensin II is known to cause renal inflammation and fibrosis. Here Lu et al. show that levels of circulating miR-103a-3p are elevated in hypertensive nephropathy patients and in an animal model of angiotensin II-induced renal dysfunction, and that miR-103a-3p suppresses SNRK expression leading to the activation of the pro-inflammatory NF-κB pathway in glomerular endothelial cells.
format	article
author	Qiulun Lu Zejun Ma Ye Ding Tatiana Bedarida Liming Chen Zhonglin Xie Ping Song Ming-Hui Zou
author_facet	Qiulun Lu Zejun Ma Ye Ding Tatiana Bedarida Liming Chen Zhonglin Xie Ping Song Ming-Hui Zou
author_sort	Qiulun Lu
title	Circulating miR-103a-3p contributes to angiotensin II-induced renal inflammation and fibrosis via a SNRK/NF-κB/p65 regulatory axis
title_short	Circulating miR-103a-3p contributes to angiotensin II-induced renal inflammation and fibrosis via a SNRK/NF-κB/p65 regulatory axis
title_full	Circulating miR-103a-3p contributes to angiotensin II-induced renal inflammation and fibrosis via a SNRK/NF-κB/p65 regulatory axis
title_fullStr	Circulating miR-103a-3p contributes to angiotensin II-induced renal inflammation and fibrosis via a SNRK/NF-κB/p65 regulatory axis
title_full_unstemmed	Circulating miR-103a-3p contributes to angiotensin II-induced renal inflammation and fibrosis via a SNRK/NF-κB/p65 regulatory axis
title_sort	circulating mir-103a-3p contributes to angiotensin ii-induced renal inflammation and fibrosis via a snrk/nf-κb/p65 regulatory axis
publisher	Nature Portfolio
publishDate	2019
url	https://doaj.org/article/fb3cafbacbca473e82a1356b6b780951
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Circulating miR-103a-3p contributes to angiotensin II-induced renal inflammation and fibrosis via a SNRK/NF-κB/p65 regulatory axis

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