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- W91366456 abstract "Cardiac hypertrophy is induced by a variety of cardiovascular diseases such as hypertension, valvular diseases, myocardial infarction, cardiomyopathy, and endocrine disorders. Although cardiac hypertrophy may be initially a beneficial response that normalizes wall stress and maintains normal cardiac function, prolonged hypertrophy becomes a leading cause of heart failure and sudden death. A number of studies have elucidated molecules responsible to the development of cardiac hypertrophy, including protein kinase C (PKC), protein kinase A (PKA), Raf-1 kinase, mitogen-activated protein (MAP) kinase family, and Janus kinase (JAK)/signal transducer and activator of transcription (STAT) family, Ras, and Rho family. It has been reported that Ca2+ regulates a number of cellular processes including cardiac hypertrophy. Since most hypertrophic signaling pathways are associated with an increase in intracellular Ca2+, Ca2+-dependent signaling pathways may be critical targets for therapies designed to prevent the progression of cardiac hypertrophy. Recently, a Ca2+/calmodulin-dependent protein kinase, and a Ca2+/calmodulin-dependent protein phosphatase, calcineurin, have attracted much attention as critical molecules that induce cardiac hypertrophy. In this review, we summarize the Ca2+-dependent signaling pathways through Ca2+/calmodulin-dependent protein kinase and calcineurin in cardiac hypertrophy." @default.
- W91366456 created "2016-06-24" @default.
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- W91366456 date "2003-01-01" @default.
- W91366456 modified "2023-09-26" @default.
- W91366456 title "Ca2+—Dependent Signaling Pathways Through Calcineurin and Ca2+ Calmodulin—Dependent Protein Kinase in Development of Cardiac Hypertrophy" @default.
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- W91366456 doi "https://doi.org/10.1007/978-1-4615-0347-7_7" @default.
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