GSNOR regulates cardiomyocyte differentiation and maturation through protein S-nitrosylation

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 o...

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Autores principales: Grimmett, Zachary W., Venetos, Nicholas M., Premont, Richard T., Stamler, Jonathan S.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: 2021
Materias:
Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8594876/
https://www.ncbi.nlm.nih.gov/pubmed/34790976
http://dx.doi.org/10.20517/jca.2021.25
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author Grimmett, Zachary W.
Venetos, Nicholas M.
Premont, Richard T.
Stamler, Jonathan S.
author_facet Grimmett, Zachary W.
Venetos, Nicholas M.
Premont, Richard T.
Stamler, Jonathan S.
author_sort Grimmett, Zachary W.
collection PubMed
description 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.
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spelling pubmed-85948762021-11-16 GSNOR regulates cardiomyocyte differentiation and maturation through protein S-nitrosylation Grimmett, Zachary W. Venetos, Nicholas M. Premont, Richard T. Stamler, Jonathan S. J Cardiovasc Aging Article 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. 2021-10-13 2021 /pmc/articles/PMC8594876/ /pubmed/34790976 http://dx.doi.org/10.20517/jca.2021.25 Text en https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, sharing, adaptation, distribution and reproduction in any medium or format, for any purpose, even commercially, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.
spellingShingle Article
Grimmett, Zachary W.
Venetos, Nicholas M.
Premont, Richard T.
Stamler, Jonathan S.
GSNOR regulates cardiomyocyte differentiation and maturation through protein S-nitrosylation
title GSNOR regulates cardiomyocyte differentiation and maturation through protein S-nitrosylation
title_full GSNOR regulates cardiomyocyte differentiation and maturation through protein S-nitrosylation
title_fullStr GSNOR regulates cardiomyocyte differentiation and maturation through protein S-nitrosylation
title_full_unstemmed GSNOR regulates cardiomyocyte differentiation and maturation through protein S-nitrosylation
title_short GSNOR regulates cardiomyocyte differentiation and maturation through protein S-nitrosylation
title_sort gsnor regulates cardiomyocyte differentiation and maturation through protein s-nitrosylation
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8594876/
https://www.ncbi.nlm.nih.gov/pubmed/34790976
http://dx.doi.org/10.20517/jca.2021.25
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