The roles of PKC-δ and PKC-ε in myocardial ischemia/reperfusion injury.

Pharmacological Research : the Official Journal of the Italian Pharmacological Society
Li ChenMing Guo

Abstract

Ischemia and reperfusion (I/R) cause a reduction in arterial blood supply to tissues, followed by the restoration of perfusion and consequent reoxygenation. The reestablishment of blood flow triggers further damage to ischemic tissue through reactive oxygen species (ROS) accumulation, interference with cellular ion homeostasis, opening of mitochondrial permeability transition pores (mPTPs) and promotion of cell death (apoptosis or necrosis). PKC-δ and PKC-ε, belonging to a family of serine/threonine kinases, have been demonstrated to play important roles during I/R injury in cardiovascular diseases. However, the cardioprotective mechanisms of PKC-δ and PKC-ε in I/R injury have not been elaborated until now. This article discusses the roles of PKC-δ and PKC-ε during myocardial I/R in redox regulation (redox signaling and oxidative stress), cell death (apoptosis and necrosis), Ca2+ overload, and mitochondrial dysfunction.

References

Aug 29, 1998·The Journal of Biological Chemistry·J ZhaoM S Marber
Oct 29, 2000·FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology·A T SaurinM S Marber
Feb 17, 2001·American Journal of Physiology. Heart and Circulatory Physiology·R M FryerG J Gross
Jun 19, 2001·American Journal of Physiology. Heart and Circulatory Physiology·H LiuZ Yao
Sep 13, 2001·Proceedings of the National Academy of Sciences of the United States of America·L ChenD Mochly-Rosen
Mar 15, 2002·American Journal of Physiology. Heart and Circulatory Physiology·Huiping LiuZhenhai Yao
Jun 14, 2002·American Journal of Physiology. Heart and Circulatory Physiology·Mitsuhiro KudoMuhammad Ashraf
Jun 14, 2002·American Journal of Physiology. Heart and Circulatory Physiology·Yoshito OhnumaKazuaki Shimamoto
Jun 10, 2003·American Journal of Physiology. Heart and Circulatory Physiology·Ting Cun Zhao, Rakesh C Kukreja
Feb 12, 2004·Journal of Molecular and Cellular Cardiology·Kimberly N GregoryEvangelia G Kranias
Feb 14, 2004·Cardiovascular Research·Andrew P HalestrapSabzali A Javadov
Jul 28, 2004·American Journal of Physiology. Heart and Circulatory Physiology·Manuel MayrQingbo Xu
Oct 27, 2004·Anesthesia and Analgesia·Shinji KohroZeljko J Bosnjak
Dec 4, 2004·American Journal of Physiology. Heart and Circulatory Physiology·Jan NeckárFrantisek Kolár
Jun 11, 2005·FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology·Paul R HanlonElizabeth Murphy
Aug 2, 2005·American Journal of Physiology. Heart and Circulatory Physiology·Ken YamamuraElizabeth Murphy
Feb 17, 2006·Basic Research in Cardiology·James M Downey, Michael V Cohen
Aug 29, 2006·American Journal of Physiology. Heart and Circulatory Physiology·Frantisek KolárJan Herget

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Citations

Oct 16, 2021·Cardiovascular Drugs and Therapy·Sumon RoyIon S Jovin

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