The Oxygen-Rich Postnatal Environment Induces Cardiomyocyte Cell-Cycle Arrest through DNA Damage Response
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- 作者：Bao N. Puente1 ; 3 ; 12 ; Wataru Kimura1 ; 12 ; Shalini A. Muralidhar1 ; Jesung Moon3 ; James F. Amatruda1 ; 2 ; 3 ; Kate L. Phelps4 ; David Grinsfelder5 ; Beverly A. Rothermel1 ; 2 ; Rui Chen1 ; Joseph A. Garcia1 ; Celio X. Santos7 ; SuWannee Thet1 ; Eiichiro Mori6 ; Michael T. Kinter8 ; Paul M. Rindler8 ; Serena Zacchigna9 ; Shibani Mukherjee6 ; David J. Chen6 ; Ahmed I. Mahmoud11 ; Mauro Giacca9 ; Peter S. Rabinovitch10 ; Aroumougame Asaithamby6 ; Ajay M. Shah7 ; Luke I. Szweda8 ; Hesham A. Sadek1 ; hesham.sadek@utsouthwestern.edu" class="auth_mail
- 刊名：Cell
- 出版年：24 April 2014
- 年：2014
- 卷：157
- 期：3
- 页码：565-579
- 全文大小：6843 K
文摘
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Mitochondrial mass and activity significantly increase in the heart after birth
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ROS and DNA damage response concomitantly increase in cardiomyocytes postnatally
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Hypoxia delays cardiomyocyte cell-cycle arrest, whereas hyperoxia potentiates it
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Scavenging ROS or inhibiting DNA damage response delays cell-cycle arrest