Key result
Nitric oxide and its synthases play crucial roles in cardiomyogenesis, modulating proliferation, differentiation, and cardiac function in both embryonic and adult mammalian hearts.
This review summarizes the evolving role of nitric oxide synthases in cardiomyogenesis and adult cardiac function, highlighting their impact on both normal development and pathophysiological states.
Should not yet change clinical practice in cardiac regeneration; leaves open targeted human studies on nitric oxide modulation.
Nitric oxide (NO) is an important signalling molecule that plays a relevant role in different cell systems, among them the adult heart. The effects of NO are primarily mediated through modulation of Ca(2+) homeostasis, myofibrillar contractility, and metabolic regulation in cardiomyocytes. Recent evidence also suggests an important role of NO for cardiomyogenesis by modulating proliferation and differentiation and regulating cardiac function. In the embryonic, but also the healthy and diseased, adult mammalian heart, the inducible (iNOS) and the endothelial (eNOS) nitric oxide synthases (NOS) are detected. However, the expression pattern of NO and its function differ during development. Furthermore, under pathophysiological conditions NOS expression can also change and cause impairment of cardiac performance and cytotoxic effects. The present review focuses on the role and function of NO during cardiomyogenesis, the mechanisms responsible for eNOS availability, and the paracrine effects of NO generated by cardiomyocytes.
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Bloch et al. (2001) conducted a review in Cardiomyogenesis and cardiac function. Nitric oxide (NO) and nitric oxide synthases (NOS) was evaluated. Nitric oxide and its synthases play crucial roles in cardiomyogenesis, modulating proliferation, differentiation, and cardiac function in both embryonic and adult mammalian hearts.
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