| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 8475340 | Journal of Molecular and Cellular Cardiology | 2013 | 8 Pages |
Abstract
⺠Dilated cardiomyopathy is an inevitable complication of Duchenne Muscular Dystrophy. ⺠Here we review recent studies on identified disease mechanisms on the cellular level. ⺠The disease is associated with cellular oxidative stress and abnormal Ca2 + signaling. ⺠Targeting these alterations may offer new treatment options in the future.
Keywords
ECCNa+–Ca2 + exchangerTRPCCa2 +-induced Ca2 + releaseCAV3NCXDMDRyRpKaCaMKIIRNSNOSSACPDEACECa2 +/calmodulin-dependent protein kinase IINOxROSangiotensin converting enzymeISOisoproterenolExcitation–contraction couplingDuchenne muscular dystrophySarcoplasmic reticulumSOCPhosphodiesteraseSERCAnitric oxide synthasenicotinamide adenine dinucleotide phosphate-oxidaseprotein kinase Acaveolin 3Transient receptor potential channelStretch-activated channelCICRreactive nitrogen speciesReactive oxygen speciesRyanodine receptor
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Authors
Natalia Shirokova, Ernst Niggli,