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Phosphorylation of smooth muscle 22α facilitates angiotensin II-induced ROS production via activation of the PKCδ-P47phox axis through release of PKCδ and actin dynamics and is associated with hypertrophy and hyperplasia of vascular smooth muscle cells in vitro and in vivo.

Authors
  • Lv, Pin
  • Miao, Sui-Bing
  • Shu, Ya-Nan
  • Dong, Li-Hua
  • Liu, George
  • Xie, Xiao-Li
  • Gao, Min
  • Wang, Yu-Can
  • Yin, Ya-Juan
  • Wang, Xiao-Juan
  • Han, Mei
Type
Published Article
Journal
Circulation Research
Publisher
Ovid Technologies (Wolters Kluwer Health)
Publication Date
Aug 31, 2012
Volume
111
Issue
6
Pages
697–707
Identifiers
DOI: 10.1161/CIRCRESAHA.112.272013
PMID: 22798525
Source
Medline
License
Unknown

Abstract

These findings indicate that the disruption of SM22α plays pivotal roles in vascular oxidative stress. PKCδ-mediated SM22α phosphorylation is a novel link between actin cytoskeletal remodeling and oxidative stress and may be a potential target for the development of new therapeutics for cardiovascular diseases.

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