期刊
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY
卷 48, 期 5, 页码 824-833出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.yjmcc.2010.01.011
关键词
Sudden cardiac death; Reentry arrhythmias; Conduction velocity; Ca2+ handling; Energetic deficit; Mechanical stretch
资金
- NHLBI NIH HHS [R01 HL071670, R01 HL071670-06A2, R01 HL088635, R01 HL088635-03] Funding Source: Medline
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL088635, R01HL071670] Funding Source: NIH RePORTER
Increased myofilament Ca2+ sensitivity is a common attribute of many inherited and acquired cardiomyopathies that are associated with cardiac arrhythmias. Accumulating evidence supports the concept that increased myofilament Ca2+ sensitivity is an independent risk factor for arrhythmias. This review describes and discusses potential underlying molecular and cellular mechanisms how myofilament Ca2+ sensitivity affects cardiac excitation and leads to the generation of arrhythmias. Emphasized are downstream effects of increased myofilament Ca2+ sensitivity: altered Ca2+ buffering/handling, impaired energy metabolism and increased mechanical stretch, and how they may contribute to arrhythmogenesis. (C) 2010 Elsevier Ltd. All rights reserved.
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