The imbalanced redox status in senescent endothelial cells is due to dysregulated Thioredoxin-1 and NADPH oxidase 4
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- 作者：Christine Goyb ; 1 ; christinegoy100@gmail.com" class="auth_mail ; Philip Czypiorskib ; 1 ; czypiorski@gmail.com" class="auth_mail ; Joachim Altschmiedb ; 1 ; Joachim.Altschmied@uni-duesseldorf.de" class="auth_mail ; Sascha Jakobb ; Sascha.Jakob@uni-duesseldorf.de" class="auth_mail ; Lothar L. Rabanterb ; Lothar.Rabanter@uni-duesseldorf.de" class="auth_mail ; Alison C. Brewerc ; alison.brewer@kcl.ac.uk" class="auth_mail ; Niloofar Ale-Aghab ; Niloofar.Ale-Agha@uni-duesseldorf.de" class="auth_mail ; Nadine Dyballa-Rukesb ; Nadine.Dyballa@uni-duesseldorf.de" class="auth_mail ; Ajay M. Shahc ; ajay.shah@kcl.ac.uk" class="auth_mail ; Judith Haendelera ; b ; juhae001@uni-duesseldorf.de" class="auth_mail
- 关键词：ROS ; reactive oxygen species ; NOXs ; NADPH oxidases ; Trx-1 ; Thioredoxin-1 ; SA ; senescence associated
- 刊名：Experimental Gerontology
- 出版年：August 2014
- 年：2014
- 卷：56
- 期：Complete
- 页码：45-52
- 全文大小：1101 K
文摘
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ROS are increased in stress-induced premature senescence in primary endothelial cells.
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Redox homeostasis is imbalanced by upregulation of NOX4 and degradation of Trx-1.
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“Over-activated” Cathepsin D increases senescence, ROS formation and Trx-1 degradation.
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Trx-1 protein levels also correlate negatively with NOX4 expression in vivo.