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- W4210535579 endingPage "416" @default.
- W4210535579 startingPage "416" @default.
- W4210535579 abstract "The most common clinical tachyarrhythmia, atrial fibrillation (AF), is present in 1-2% of the population. Although common risk factors, including hypertension, diabetes, and obesity, frequently underlie AF onset, it has been recognized that in 15% of the AF population, AF is familial. In these families, genome and exome sequencing techniques identified variants in the non-coding genome (i.e., variant regulatory elements), genes encoding ion channels, as well as genes encoding cytoskeletal (-associated) proteins. Cytoskeletal protein variants include variants in desmin, lamin A/C, titin, myosin heavy and light chain, junctophilin, nucleoporin, nesprin, and filamin C. These cytoskeletal protein variants have a strong association with the development of cardiomyopathy. Interestingly, AF onset is often represented as the initial manifestation of cardiac disease, sometimes even preceding cardiomyopathy by several years. Although emerging research findings reveal cytoskeletal protein variants to disrupt the cardiomyocyte structure and trigger DNA damage, exploration of the pathophysiological mechanisms of genetic AF is still in its infancy. In this review, we provide an overview of cytoskeletal (-associated) gene variants that relate to genetic AF and highlight potential pathophysiological pathways that drive this arrhythmia." @default.
- W4210535579 created "2022-02-08" @default.
- W4210535579 creator A5015228772 @default.
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- W4210535579 creator A5035027228 @default.
- W4210535579 creator A5044231856 @default.
- W4210535579 creator A5062443343 @default.
- W4210535579 date "2022-01-25" @default.
- W4210535579 modified "2023-10-04" @default.
- W4210535579 title "Cytoskeletal Protein Variants Driving Atrial Fibrillation: Potential Mechanisms of Action" @default.
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