Gap junctions mediate the spread of ischemia-reperfusion injury.
Gap junctions mediate the spread of ischemia-reperfusion injury.
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DOI:
10.1253/circj.cj-09-0342
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发表时间:
2009-08
期刊:
影响因子:
--
通讯作者:
T. Minamino
中科院分区:
文献类型:
--
作者:
T. Minamino
ap junctions are clusters of transmembrane channels that form conduits for direct intercellular communication by linking the cytoplasmic compartments of neighboring cells.1 Gap junctional intercellular communications play a key role in tissue homeostasis and in the regulation of growth, differentiation, and development. In the heart, gap junctions mediate electrical coupling between cardiomyocytes, forming the intercellular pathways that allow orderly spread of the wave of electrical excitation responsible for synchronous contraction. Therefore, the normal cardiac rhythm largely depends on the coupling of cardiomyocytes by gap junctions. Disturbance of the cardiac rhythm is a common, serious, and often fatal complication of many types of heart disease. Although abnormalities of the membrane properties responsible for the active potential play a central role in the genesis of arrhythmia, evidence suggests that impaired gap junction function also contributes to cardiac arrhythmia. Therefore, the influence of abnormal gap junction function on myocardial electrical behavior has been extensively investigated. In contrast, although it is known that gap junctions also allow the diffusion of small molecules, the pathological significance of such chemical coupling has attracted relatively little attention.