Cardiac robustness regulated by reactive sulfur species

The human myocardium contains robust cells that constantly beat from birth to death without being replaced, even when exposed to various environmental stresses. Myocardial robustness is thought to depend primarily on the strength of the reducing power to protect the heart from oxidative stress. Myoc...

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Bibliographic Details
Published in:Journal of Clinical Biochemistry and Nutrition 2022, Vol.70(1), pp.1-6
Main Authors: Nishimura, Akiyuki, Tanaka, Tomohiro, Kato, Yuri, Nishiyama, Kazuhiro, Nishida, Motohiro
Format: Article
Language:English
Subjects:
Antioxidants
cardiac senescence
Congestive heart failure
Electron transfer
electrophile
Energy metabolism
Environmental stress
Glutathione
Mitochondria
mitochondrial quality control
Molecular modelling
Myocardium
Oxidative stress
persulfide
Quality control
reactive sulfide species
Redox reactions
Robustness
Serial Review
Species
Sulfhydryl groups
Sulfides
Sulfur
Thioredoxin
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Summary:The human myocardium contains robust cells that constantly beat from birth to death without being replaced, even when exposed to various environmental stresses. Myocardial robustness is thought to depend primarily on the strength of the reducing power to protect the heart from oxidative stress. Myocardial antioxidant systems are controlled by redox reactions, primarily via the redox reaction of Cys sulfhydryl groups, such as found in thioredoxin and glutathione. However, the specific molecular entities that regulate myocardial reducing power have long been debated. Recently, reactive sulfide species, with excellent electron transfer ability, consisting of a series of multiple sulfur atoms, i.e., Cys persulfide and Cys polysulfides, have been found to play an essential role in maintaining mitochondrial quality and function, as well as myocardial robustness. This review presents the latest findings on the molecular mechanisms underlying mitochondrial energy metabolism and the maintenance of quality control by reactive sulfide species and provides a new insight for the prevention of chronic heart failure.
ISSN:0912-0009
1880-5086
DOI:10.3164/jcbn.21-84