Maintenance of small molecule redox homeostasis in mitochondria
Compartmentalisation of eukaryotic cells enables fundamental otherwise often incompatible cellular processes. Establishment and maintenance of distinct compartments in the cell relies not only on proteins, lipids and metabolites but also on small redox molecules. In particular, small redox molecules...
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Published in | FEBS letters Vol. 597; no. 2; pp. 205 - 223 |
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Main Authors | , |
Format | Journal Article |
Language | English |
Published |
England
01.01.2023
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Subjects | |
Online Access | Get full text |
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Summary: | Compartmentalisation of eukaryotic cells enables fundamental otherwise often incompatible cellular processes. Establishment and maintenance of distinct compartments in the cell relies not only on proteins, lipids and metabolites but also on small redox molecules. In particular, small redox molecules such as glutathione, NAD(P)H and hydrogen peroxide (H2O2) cooperate with protein partners in dedicated machineries to establish specific subcellular redox compartments with conditions that enable oxidative protein folding and redox signalling. Dysregulated redox homeostasis has been directly linked with a number of diseases including cancer, neurological disorders, cardiovascular diseases, obesity, metabolic diseases and ageing. In this review, we will summarise mechanisms regulating establishment and maintenance of redox homeostasis in the mitochondrial subcompartments of mammalian cells.
Compartmentalisation of eukaryotic cells allows for the execution of seemingly incompatible cellular processes. Establishment and maintenance of compartmental identity require partitioning of proteins, lipids, metabolites and small redox molecules. Dysregulated redox homeostasis has been linked with cancer, neurological disorders, cardiovascular diseases, metabolic diseases and ageing. Here, we discuss mechanisms regulating the establishment and maintenance of small redox molecule homeostasis within mitochondrial subcompartments. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-3 content type line 23 ObjectType-Review-1 |
ISSN: | 0014-5793 1873-3468 |
DOI: | 10.1002/1873-3468.14485 |