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Updated: May 12, 2026

Assessment of Sarcoplasmic Reticulum Calcium Reserve and Intracellular Diastolic Calcium Removal in Isolated Ventricular Cardiomyocytes
Published on: September 18, 2017
[Calcium dependent signaling in cardiac hypertrophy and cell death]
Hiroyuki Nakayama1, Yasushi Fujio, Osamu Yamaguchi
1Graduate School of Pharmaceutical Sciences, Osaka University, Japan.
Abstract:
Ca(2 +) plays a pivotal role in excitation-contraction coupling as well as activation of Ca(2 +) -dependent signaling pathways in the myocardium. The two main established Ca(2 +) -dependent pathways during cardiomyocyte hypertrophy are the Ca(2 +) /calmodulin-calcineurin-NFAT and the Ca(2 +) /calmodulin dependent kinases II -HDAC-MEF2. Both pathways are involved in the transcriptional control of many hypertrophic genes. Recently, cyclophilin D, an immunophilin located on mitochondrial inner membrane, has been highlighted as a regulator of calcium-mediated mitochondrial permeability transition in necrotic cardiac cell death.
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