Abstract

Reactive oxygen species (ROS) are well known for their role in mediating both physiological and pathophysiological signal transduction. Enzymes and subcellular compartments that typically produce ROS are associated with metabolic regulation, and diseases associated with metabolic dysfunction may be influenced by changes in redox balance. In this review, we summarize the current literature surrounding ROS and their role in metabolic and inflammatory regulation, focusing on ROS signal transduction and its relationship to disease progression. In particular, we examine ROS production in compartments such as the cytoplasm, mitochondria, peroxisome, and endoplasmic reticulum and discuss how ROS influence metabolic processes such as proteasome function, autophagy, and general inflammatory signaling. We also summarize and highlight the role of ROS in the regulation metabolic/inflammatory diseases including atherosclerosis, diabetes mellitus, and stroke. In order to develop therapies that target oxidative signaling, it is vital to understand the balance ROS signaling plays in both physiology and pathophysiology, and how manipulation of this balance and the identity of the ROS may influence cellular and tissue homeostasis. An increased understanding of specific sources of ROS production and an appreciation for how ROS influence cellular metabolism may help guide us in the effort to treat cardiovascular diseases.

Keywords

Reactive oxygen speciesAutophagySignal transductionCell biologyBiologyMitochondrionOxidative stressPeroxisomeCell signalingHomeostasisInflammationBiochemistryImmunologyApoptosisReceptor

MeSH Terms

AnimalsCardiovascular DiseasesHumansMetabolic DiseasesReactive Oxygen SpeciesSignal Transduction

Affiliated Institutions

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Publication Info

Year
2018
Type
review
Volume
122
Issue
6
Pages
877-902
Citations
1856
Access
Closed

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1856
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Cite This

Steven J. Forrester, Daniel S. Kikuchi, Marina S. Hernandes et al. (2018). Reactive Oxygen Species in Metabolic and Inflammatory Signaling. Circulation Research , 122 (6) , 877-902. https://doi.org/10.1161/circresaha.117.311401

Identifiers

DOI
10.1161/circresaha.117.311401
PMID
29700084
PMCID
PMC5926825

Data Quality

Data completeness: 86%