Journal
FREE RADICAL BIOLOGY AND MEDICINE
Volume 141, Issue -, Pages 483-491Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.freeradbiomed.2019.07.017
Keywords
Mitochondria; ROS; Mitohormesis; Metabolic diseases; cAMP; Sirtuin
Funding
- European Regional Development Fund, through the Centro 2020 Regional Operational Programme [CENTRO-01-0145-FEDER-000012-HealthyAging2020]
- Portugal 2020 - Operational Programme for Competitiveness and Internationalisation
- Portuguese national funds via FCT Fundacao para a Ciencia e a Tecnologia, I.P. [POCI-01-0145FEDER-016770]
- CNC. IBILI Consortium strategic project [UID/NEU/04539/2013]
- Dr. Robert Pfleger Foundation
- FCT [SFRH/BPD/94036/2013, PD/BD/114173/2016]
- NIH [R37 AG028730, R01 AG019719, R01 DK100263]
- Epigenetics Seed Grant from Department of Genetics, Harvard Medical School [601139_ 2018]
- Glenn Foundation for Medical Research
- Fundação para a Ciência e a Tecnologia [PD/BD/114173/2016] Funding Source: FCT
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The key role of mitochondria in oxidative metabolism and redox homeostasis explains the link between mitochondrial dysfunction and the development of metabolic disorders. Mitochondria's highly dynamic nature, based on alterations in biogenesis, mitophagy, fusion and fission, allows adjusting sequential redox reactions of the electron transport chain (ETC) and dissipation of the membrane potential by ATP synthase, to different environmental cues. With reactive oxygen species being an inevitable by-product of oxidative phosphorylation (OXPHOS), alterations on mitochondrial oxidative rate with a consequent excessive load of reactive oxygen species have been traditionally associated with pathological conditions. However, reactive oxygen species have also been suggested as promoters of mitohormesis, a process in which low, non-cytotoxic concentrations of reactive oxygen species promote mitochondrial homeostasis. Therefore, signaling systems involved in the regulation of mitochondrial homeostasis are attractive candidates for drug development for metabolic diseases triggered by mitochondrial dysfunction. Reversible phosphorylation downstream the cyclic AMP (cAMP) signaling cascade and deacetylation mediated by sirtuins are recognized as major mitochondrial regulators.
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