Regucalcin plays a crucial regulatory role in cardiac calcium signaling and may offer cardioprotective effects against heart failure by modulating key enzymes like SERCA2a, NO synthase, and SOD.
Should not change heart failure practice; leaves open regucalcin as a therapeutic target for future study.
Regucalcin was first identified in 1978 as a regulatory protein of Ca2+ signaling in liver cells. Regucalcin was shown to play a multifunctional role in cell regulation, such as maintainance of intracellular Ca2+ homeostasis and suppression of signal transduction, protein synthesis, nuclear function, cell proliferation and apoptosis in various types of cells and tissues. Cardiac excitation‑contraction coupling is based on the regulation of intracellular Ca2+ concentration by the Ca2+ pump in the sarcoplasmic reticulum of heart muscle cells. Regucalcin, which is expressed in the heart, was found to increase rat heart sarcoplasmic reticulum Ca2+‑ATPase activity and ATP‑dependent Ca2+ uptake and mitochondrial Ca2+‑ATPase activity. Regucalcin was also shown to suppress Ca2+‑dependent protein tyrosine phosphatase, Ca2+/calmodulin‑dependent protein phosphatase (calcineurin) and nitric oxide (NO) synthase activity in the heart cytoplasm. Moreover, regucalcin was found to activate superoxide dismutase (SOD), which plays a significant role in the prevention of cell death and apoptosis in the heart. Regucalcin may be a key molecule in heart muscle cell regulation through Ca2+ signaling. Regucalcin may also play a pathophysiological role in heart failure. The aim of this study was to review the recent findings regarding the role of regucalcin in Ca2+ signaling in the heart.
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Masayoshi Yamaguchi (2014) studied this question.
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