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Redox Signaling In The Cardiomyocyte: From Physiology To Failure

Research output: Contribution to journalArticlepeer-review

Celio XC Santos, Sadaf Raza, Ajay M Shah, FMedSci [Unknown]

Original languageEnglish
JournalInternational Journal of Biochemistry and Cell Biology
Early online date14 Mar 2016
Accepted/In press11 Mar 2016
E-pub ahead of print14 Mar 2016


  • 1-s2.0-S1357272516300565-main

    1_s2.0_S1357272516300565_main.pdf, 873 KB, application/pdf

    Uploaded date:15 Mar 2016

    Version:Accepted author manuscript

King's Authors


Abstract The specific effect of oxygen and reactive oxygen species (ROS) in mediating post-translational modification of protein targets has emerged as a key mechanism regulating signaling components, a process termed redox signaling. ROS act in the post-translational modification of multiple target proteins including receptors, kinases, phosphatases, ion channels and transcription factors. Both O2 and ROS are major source of electrons in redox reactions in aerobic organisms. Because the heart has the highest O2 consumption among body organs, it is not surprising that redox signaling is central to heart function and pathophysiology. In this article, we review some of the main cardiac redox signaling pathways and their roles in the cardiomyocyte and in heart failure, with particular focus on the specific molecular targets of ROS in the heart.

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