GSNOR通过蛋白质S-亚硝基化调节心肌细胞的分化和成熟。
GSNOR regulates cardiomyocyte differentiation and maturation through protein S-nitrosylation.
作者信息
Grimmett Zachary W, Venetos Nicholas M, Premont Richard T, Stamler Jonathan S
机构信息
Department of Pathology, Case Western Reserve University School of Medicine, Cleveland, OH 44106, USA.
Institute for Transformative Molecular Medicine, Department of Medicine, Case Western Reserve University School of Medicine, Cleveland, OH 44106, USA.
出版信息
J Cardiovasc Aging. 2021;1. doi: 10.20517/jca.2021.25. Epub 2021 Oct 13.
S-nitrosoglutathione reductase (GSNOR) is a denitrosylase enzyme responsible for reverting protein S-nitrosylation (SNO). In this issue, Salerno 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.
S-亚硝基谷胱甘肽还原酶（GSNOR）是一种去亚硝基化酶，负责逆转蛋白质S-亚硝基化（SNO）。在本期中，萨勒诺提供证据表明，GSNOR缺乏症以及由此导致的蛋白质S-亚硝基化水平升高会加速诱导多能干细胞（iPSC）的心肌细胞分化和成熟。GSNOR抑制（GSNOR-iPSC）可加速上皮-间质转化（EMT），并促进心肌祖细胞的增殖、分化和迁移。这些发现与蛋白质S-亚硝基化在发育生物学（包括心肌细胞发育）、衰老/长寿和癌症中的新作用一致。
Zotero 插件