Redox metabolism: ROS as specific molecular regulators of cell signaling and function

Redox reactions are intrinsically linked to energy metabolism. Therefore, redox processes are indispensable for organismal physiology and life itself. The term reactive oxygen species (ROS) describes a set of distinct molecular oxygen derivatives produced during normal aerobic metabolism. Multiple R...

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Veröffentlicht in:Molecular cell Jg. 81; H. 18; S. 3691
Hauptverfasser: Lennicke, Claudia, Cochemé, Helena M
Format: Journal Article
Sprache:Englisch
Veröffentlicht: United States 16.09.2021
Schlagworte:
Animals
Cysteine - metabolism
Energy Metabolism - physiology
Homeostasis
Humans
Hydrogen Peroxide - metabolism
Oxidation-Reduction
Oxidative Stress
Protein Processing, Post-Translational - physiology
Reactive Oxygen Species - metabolism
Signal Transduction - physiology
redox signaling
ROS
hydrogen peroxide
reactive oxygen species
redox metabolism
post-translational modification
cysteine oxidation
ISSN:1097-4164, 1097-4164
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Zusammenfassung:Redox reactions are intrinsically linked to energy metabolism. Therefore, redox processes are indispensable for organismal physiology and life itself. The term reactive oxygen species (ROS) describes a set of distinct molecular oxygen derivatives produced during normal aerobic metabolism. Multiple ROS-generating and ROS-eliminating systems actively maintain the intracellular redox state, which serves to mediate redox signaling and regulate cellular functions. ROS, in particular hydrogen peroxide (H O ), are able to reversibly oxidize critical, redox-sensitive cysteine residues on target proteins. These oxidative post-translational modifications (PTMs) can control the biological activity of numerous enzymes and transcription factors (TFs), as well as their cellular localization or interactions with binding partners. In this review, we describe the diverse roles of redox regulation in the context of physiological cellular metabolism and provide insights into the pathophysiology of diseases when redox homeostasis is dysregulated.
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ISSN:1097-4164
1097-4164
DOI:10.1016/j.molcel.2021.08.018