Abstract
S-nitrosoglutathione reductase (GSNOR) is a denitrosylase enzyme responsible for reverting protein S-nitrosylation (SNO). In this issue, Salerno et al.[1] provide evidence that GSNOR deficiency - and thus elevated protein S-nitrosylation - accelerates cardiomyocyte differentiation and maturation of induced pluripotent stem cells (iPSCs). GSNOR inhibition (GSNOR−/− iPSCs) expedites the epithelial-mesenchymal transition (EMT) and promotes cardiomyocyte progenitor cell proliferation, differentiation, and migration. These findings are consistent with emerging roles for protein S-nitrosylation in developmental biology (including cardiomyocyte development), aging/longevity, and cancer.
Highlights
S-nitrosoglutathione reductase (GSNOR) is a denitrosylase enzyme responsible for reverting protein Snitrosylation (SNO)
GSK-3β is an essential kinase with multiple roles, in cardiovascular physiology[4]
GSNOR-dependent SNO-targets beyond GSK-3β may contribute to altered cardiomyocyte differentiation, and denitrosylases other than GSNOR may play important roles
Summary
S-nitrosoglutathione reductase (GSNOR) is a denitrosylase enzyme responsible for reverting protein Snitrosylation (SNO). Salerno et al.[1] provide evidence that GSNOR deficiency - and elevated protein S-nitrosylation - accelerates cardiomyocyte differentiation and maturation of induced pluripotent stem cells (iPSCs). These findings are consistent with emerging roles for protein S-nitrosylation in developmental biology (including cardiomyocyte development), aging/longevity, and cancer.
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