Dynamic Regulation of Cysteine Oxidation and Phosphorylation in Myocardial Ischemia-Reperfusion Injury.

Dynamic Regulation of Cysteine Oxidation and Phosphorylation in Myocardial Ischemia-Reperfusion Injury.
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半胱氨酸氧化和磷酸化在心肌缺血再灌注损伤中的动态调节。

DOI:
10.3390/cells10092388
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发表时间:
2021-09-11
期刊:
影响因子:
6
通讯作者:
Calvert JW
Calvert JW
中科院分区:
生物学2区
文献类型:
--
作者:
Casin KM;Calvert JW

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心肌缺血-再灌注(I/R)损伤显著改变了梗死后的心功能,并增加了心力衰竭的风险。许多研究都试图保护不可替代的心肌,称为心脏保护,但很少有,如果有的话,治疗已经产生了临床I/R损伤的大幅减少。需要更多的研究来充分了解控制心脏保护的分子途径。氧化还原机制,特别是半胱氨酸氧化,是由激酶介导的分子信号级联的急性和关键调节剂。在这里,我们回顾了活性氧在修饰半胱氨酸残基中的作用,以及这些修饰如何影响激酶功能以影响心脏保护。这一令人兴奋的研究领域可能会为机制提供新的见解,并可能导致I/R损伤的新治疗方法。
Myocardial ischemia–reperfusion (I/R) injury significantly alters heart function following infarct and increases the risk of heart failure. Many studies have sought to preserve irreplaceable myocardium, termed cardioprotection, but few, if any, treatments have yielded a substantial reduction in clinical I/R injury. More research is needed to fully understand the molecular pathways that govern cardioprotection. Redox mechanisms, specifically cysteine oxidations, are acute and key regulators of molecular signaling cascades mediated by kinases. Here, we review the role of reactive oxygen species in modifying cysteine residues and how these modifications affect kinase function to impact cardioprotection. This exciting area of research may provide novel insight into mechanisms and likely lead to new treatments for I/R injury.
DOI: 10.1161/atvbaha.112.251769
发表时间: 2012-08
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