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S-glutathionylation, friend or foe in cardiovascular health and disease

Glutathione is a low molecular weight thiol that is present at high levels in the cell. The high levels of glutathione in the cell make it one of the most abundant antioxidants contributing to cellular redox homeostasis. As a general rule, throughout cardiovascular disease and progression there is a...

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Detalles Bibliográficos
Autores principales: Rashdan, N.A., Shrestha, B., Pattillo, C.B.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7767732/
https://www.ncbi.nlm.nih.gov/pubmed/32912836
http://dx.doi.org/10.1016/j.redox.2020.101693
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author Rashdan, N.A.
Shrestha, B.
Pattillo, C.B.
author_facet Rashdan, N.A.
Shrestha, B.
Pattillo, C.B.
author_sort Rashdan, N.A.
collection PubMed
description Glutathione is a low molecular weight thiol that is present at high levels in the cell. The high levels of glutathione in the cell make it one of the most abundant antioxidants contributing to cellular redox homeostasis. As a general rule, throughout cardiovascular disease and progression there is an imbalance in redox homeostasis characterized by reactive oxygen species overproduction and glutathione underproduction. As research into these imbalances continues, glutathione concentrations are increasingly being observed to drive various physiological and pathological signaling responses. Interestingly in addition to acting directly as an antioxidant, glutathione is capable of post translational modifications (S-glutathionylation) of proteins through both chemical interactions and enzyme mediated events. This review will discuss both the chemical and enzyme-based S-glutathionylation of proteins involved in cardiovascular pathologies and angiogenesis.
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spelling pubmed-77677322020-12-29 S-glutathionylation, friend or foe in cardiovascular health and disease Rashdan, N.A. Shrestha, B. Pattillo, C.B. Redox Biol Review Article Glutathione is a low molecular weight thiol that is present at high levels in the cell. The high levels of glutathione in the cell make it one of the most abundant antioxidants contributing to cellular redox homeostasis. As a general rule, throughout cardiovascular disease and progression there is an imbalance in redox homeostasis characterized by reactive oxygen species overproduction and glutathione underproduction. As research into these imbalances continues, glutathione concentrations are increasingly being observed to drive various physiological and pathological signaling responses. Interestingly in addition to acting directly as an antioxidant, glutathione is capable of post translational modifications (S-glutathionylation) of proteins through both chemical interactions and enzyme mediated events. This review will discuss both the chemical and enzyme-based S-glutathionylation of proteins involved in cardiovascular pathologies and angiogenesis. Elsevier 2020-08-22 /pmc/articles/PMC7767732/ /pubmed/32912836 http://dx.doi.org/10.1016/j.redox.2020.101693 Text en © 2020 Published by Elsevier B.V. http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
spellingShingle Review Article
Rashdan, N.A.
Shrestha, B.
Pattillo, C.B.
S-glutathionylation, friend or foe in cardiovascular health and disease
title S-glutathionylation, friend or foe in cardiovascular health and disease
title_full S-glutathionylation, friend or foe in cardiovascular health and disease
title_fullStr S-glutathionylation, friend or foe in cardiovascular health and disease
title_full_unstemmed S-glutathionylation, friend or foe in cardiovascular health and disease
title_short S-glutathionylation, friend or foe in cardiovascular health and disease
title_sort s-glutathionylation, friend or foe in cardiovascular health and disease
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7767732/
https://www.ncbi.nlm.nih.gov/pubmed/32912836
http://dx.doi.org/10.1016/j.redox.2020.101693
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