Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8270787 | Free Radical Biology and Medicine | 2013 | 12 Pages |
Abstract
In this review article we give an overview of current knowledge with respect to redox-sensitive alterations in Na+ and Ca2+ 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 Ca2+ 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 Ca2+ imbalance will be given.
Keywords
NADPHITIA-kinase anchor proteinBH4tetrahydrobiopterinMPTCaMKIINOS1NOS2NOSAPDDADFKBP12.6NHEGSHEADHFrEFHFpEFNav1.5LTCCNOS3DCMAKAPNCX1ECCICADOXNKAcAMPINaNa+/H+ exchangerCyclic adenosine monophosphateAngiotensin IImitochondrial permeability transitionearly afterdepolarizationsITOExcitation-contraction couplingTransient inward currentAng IIDoxorubicindiacylglycerolDAGCAMendoplasmic reticulumAction potential durationNADHHeart failure with preserved ejection fractionheart failureheart failure with reduced ejection fractionNitric oxidenitric oxide synthasenicotinamide adenine dinucleotidenicotinamide adenine dinucleotide phosphateETcaction potentialdelayed afterdepolarizationDilated cardiomyopathyCalmodulinL-type Ca2+ channelsGluthathione
Related Topics
Life Sciences
Biochemistry, Genetics and Molecular Biology
Ageing
Authors
Can M. Sag, Stefan Wagner, Lars S. Maier,