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New Protective Roles of ROS against Myocardial Ischemia/Reperfusion Identified

Mar 17, 2015     Email"> PrintText Size

Though early reperfusion during myocardial infarction is essential for saving the myocardium, lethal reperfusion injury occurs and contributes to cardiac dysfunction and infarction. Ca2+ overloading and the increase of reactive oxygen species (ROS) production are considered as two major injury factors from ischemia/reperfusion (I/R) injury. However, ROS also participate in protective signal transduction and ischemic preconditioning (IPC)/postconditioning (IPoC)-induced cardioprotection against I/R injury. Therefore, it is important to further understand the role and mechanisms of ROS during the I/R injury and cardioprotection to promote the development new strategies for cardiac protection.

Recently a team of researchers, led by Prof. YANG, at the Institute of Health Science (IHS), found a new mechanism of the cardioprotection from the ROS during I/R injury with a cardiac protective model of intermittent hypobaric hypoxia (IHH). During early reperfusion, the enhanced ROS plays an important role in the IHH-afforded cardioprotection against I/R-induced Ca2+ overload and contractile dysfunction through the effective activation of JAK2/STAT3 pathway. Such protection is due to the improvement of sarcoplasmic reticulum Ca2+-ATPase 2 (SERCA2) activity via the increase in the SR Bcl-2 expression and its interaction with the SERCA2. Meanwhile, the enhanced ROS during early reperfusion by IHH reverses I/R-suppressed STAT3 phosphorylation in mitochondria and mitochondrial membrane potential.

These findings clearly conveys a mechanism by which ROS activates JAK/STAT to increase SERCA2 activity and decrease resting Ca2+, as well as I/R injury. This study makes a contribution to the literature by offering a mechanistic explanation for how ROS may contribute to cardioprotection against IR injury.

This study was published on Journal of Molecular and Cellular Cardiology on Feb. 27, 2015, and was supported by the Major State Basic Research Development Program of China, National Natural Sciences Foundation of China, and National Science and Technology Major Project of China.

CONTACT:
YANG Huangtian
Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences and Shanghai Jiao Tong University School of Medicine 
Shanghai 200031, China.
E-mail: htyang@sibs.ac.cn 

Attachment:

(Editor: CHEN Na)

Contact

YANG Huangtian

Institute of Health Sciences, Shanghai Institutes for Biological Sciences

Phone:
E-mail: htyang@sibs.ac.cn

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