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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.

作者:Can M, Sag;Stefan, Wagner;Lars S, Maier

来源:Free radical biology & medicine 2013 年 63卷

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收藏
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作者:
Can M, Sag;Stefan, Wagner;Lars S, Maier
来源:
Free radical biology & medicine 2013 年 63卷
标签:
(late), late Na(+) current A-kinase anchor protein AKAP AP APD Ang II BH4 Ca handling Ca/calmodulin-dependent protein kinase II CaM CaMKII CaMKIIδ(C) Calcium Coupling DAD DAG DCM DOX EAD ECC ER ETC Exciation—contraction FKBP12.6 GSH HF HFpEF HFrEF I(Ca) I(Na) I(Ti) I(to) L-type Ca(2+) channels LTCC Late Na current MPT NADH NADPH NADPH oxidase NCX1 NHE NKA NO NOS NOS1 NOS2 NOS3 NOX Na(+) channel protein Na(+)/H(+) exchanger NaV1.5 ONOO(-) PKA PKC PLB PLM PPI-1 ROS RyR2 SERCA2a SOD SR SR Ca leak Sodium Trx XOR action potential action potential duration angiotensin II cAMP cAMP-dependent protein kinase A calmodulin calstabin cyclic adenosine monophosphate cytosolic splice variant of Ca/calmodulin-dependent protein kinase II delayed afterdepolarization diacylglycerol dilated cardiomyopathy doxorubicin early afterdepolarizations electron transport chain in the mitochondria endoplasmic reticulum endothelial nitric oxide synthase (also eNOS) excitation-contraction coupling gluthathione heart failure heart failure with preserved ejection fraction heart failure with reduced ejection fraction inducible nitric oxide synthase (also iNOS) inward Ca(2+) current inward Na(+) current mitochondrial permeability transition neuronal nitric oxide synthase (also nNOS) nicotinamide adenine dinucleotide nicotinamide adenine dinucleotide phosphate nitric oxide nitric oxide synthase outward rectifying K(+) currents peroxynitrite phospholamban phospholemman protein kinase C protein phosphatase inhibitor 1 reactive oxygen species ryanodine receptors sarcolemmal Na(+)/Ca(2+) exchanger sarcolemmal Na(+)/K(+) ATPase sarcoplasmic reticulum sarcoplasmic reticulum Ca(2+)-ATPase superoxide dismutase tetrahydrobiopterin thioredoxin transient inward current xanthine oxidase
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.