Cardiovascular Division, The James Black Centre, King's College London, UK.
Free Radic Biol Med. 2013 Oct;63:338-49. doi: 10.1016/j.freeradbiomed.2013.05.035. Epub 2013 Jun 1.
In this review article we give an overview of current knowledge with respect to redox-sensitive alterations in Na(+) and Ca(2+) handling in the heart. In particular, we focus on redox-activated protein kinases including cAMP-dependent protein kinase A (PKA), protein kinase C (PKC), and Ca/calmodulin-dependent protein kinase II (CaMKII), as well as on redox-regulated downstream targets such as Na(+) and Ca(2+) transporters and channels. We highlight the pathological and physiological relevance of reactive oxygen species and some of its sources (such as NADPH oxidases, NOXes) for excitation-contraction coupling (ECC). A short outlook with respect to the clinical relevance of redox-dependent Na(+) and Ca(2+) imbalance will be given.
在这篇综述文章中,我们概述了目前关于心脏中钠(Na(+))和钙(Ca(2+))处理的氧化还原敏感改变的知识。特别是,我们关注氧化还原激活的蛋白激酶,包括环腺苷酸依赖性蛋白激酶 A(PKA)、蛋白激酶 C(PKC)和钙/钙调蛋白依赖性蛋白激酶 II(CaMKII),以及氧化还原调节的下游靶标,如 Na(+)和 Ca(2+)转运体和通道。我们强调了活性氧及其一些来源(如 NADPH 氧化酶、NOXes)对兴奋-收缩偶联(ECC)的病理和生理相关性。还简要展望了氧化还原依赖的 Na(+)和 Ca(2+)失衡的临床相关性。