Coenzyme Q redox signalling and longevity

Scialò, Filippo; Sanz, Alberto

doi:10.1016/j.freeradbiomed.2021.01.018

Cited by 29 publications

(24 citation statements)

References 246 publications

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“…Under TS, in young mitochondria ROS-RET is activated in response to increased electron entry through CI/CII and accessory dehydrogenases that are not part of the canonical ETC. This is similar to what has been reported in other scenarios where ROS-RET is triggered [ 38 ]. For example, ROS-RET is usually associated with increased oxidation of succinate by CII, like during ischemia reperfusion [ 6 ] or hypoxia within specialised cells of the carotid body [ 10 ].…”

Section: Discussionsupporting

confidence: 91%

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Mitochondrial ROS signalling requires uninterrupted electron flow and is lost during ageing in flies

et al. 2022

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Mitochondrial reactive oxygen species (mtROS) are cellular messengers essential for cellular homeostasis. In response to stress, reverse electron transport (RET) through respiratory complex I generates high levels of mtROS. Suppression of ROS production via RET (ROS-RET) reduces survival under stress, while activation of ROS-RET extends lifespan in basal conditions. Here, we demonstrate that ROS-RET signalling requires increased electron entry and uninterrupted electron flow through the electron transport chain (ETC). We find that in old fruit flies, ROS-RET is abolished when electron flux is decreased and that their mitochondria produce consistently high levels of mtROS. Finally, we demonstrate that in young flies, limiting electron exit, but not entry, from the ETC phenocopies mtROS generation observed in old individuals. Our results elucidate the mechanism by which ROS signalling is lost during ageing.

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Section: Discussionsupporting

confidence: 91%

“…During ageing, there is an increase in the generation of mtROS [ 38 ] that will impact redox signalling. Here, we show that young mitochondria increase ROS production in response to specific stimuli such as TS and rotenone, while aged mitochondria continually produce high levels of ROS (Fig.…”

Section: Discussionmentioning

confidence: 99%

Mitochondrial ROS signalling requires uninterrupted electron flow and is lost during ageing in flies

et al. 2022

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“…ROS act as regulatory and signalling molecules and are essential to proper cell function in a system known as REDOX regulation [19], participating in cell division, differentiation, and death. Consequently, OS also produces dysregulation of the redox signalling, and therefore, an alteration in cellular homeostasis [20,21].…”

Section: What Is Oxidative Stress?mentioning

confidence: 99%

Oxidative Stress and Endoplasmic Reticulum Stress in Rare Respiratory Diseases

Magallón

Carrión

Bañuls

et al. 2021

JCM

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Several studies have shown that some rare respiratory diseases, such as alpha-1 antitrypsin deficiency (AATD), idiopathic pulmonary fibrosis (IPF), cystic fibrosis (CF), and primary ciliary dyskinesia (PCD) present oxidative stress (OS) and endoplasmic reticulum (ER) stress. Their involvement in these pathologies and the use of antioxidants as therapeutic agents to minimize the effects of OS are discussed in this review.

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“…During ageing we propose that CI ceases to be the main ROS generator and is replaced by one or more generators inactive in young flies. The most likely candidate is CIII which has been shown to increase ROS when CIV is inhibited and has been described as the main generator of ROS in aged rat heart mitochondria [23][24][25]. Further research to confirm or discard this possibility is warranted.…”

Section: Discussionmentioning

confidence: 99%

ROS signalling requires uninterrupted electron flow and is lost during ageing in flies

Graham

Stefanatos

Yek

et al. 2021

Preprint

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Mitochondrial Reactive Oxygen Species (mtROS) are cellular messengers essential for cellular homeostasis. In response to stress, reverse electron transport (RET) by respiratory complex I generates high levels of mtROS. Suppression of ROS produced via RET (ROS-RET) reduces survival under stress, while activation of ROS-RET extends lifespan in basal conditions. Here, we demonstrate that ROS-RET signalling requires increased electron entry and uninterrupted electron flow through the electron transport chain (ETC). We found that ROS-RET is abolished in old fruit flies where electron flux is reduced. Instead, mitochondria in aged flies produce consistently high levels of mtROS. Finally, we demonstrate that in young flies reduction of electron exit from the ETC, but not electron entry, phenocopies mtROS generation observed in old individuals. Our results define the mechanism by which ROS signalling is lost during ageing.HighlightsROS-RET signalling requires an uninterrupted flow of electrons through the ETC.ROS-RET signalling fails during ageing, with mitochondria producing persistently high levels of ROS.Interruption of ROS-RET signalling compromises stress adaptation in old flies.Reducing electron exit suppresses ROS-RET signalling and phenocopies ROS production observed in old mitochondria.

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Coenzyme Q redox signalling and longevity

Cited by 29 publications

References 246 publications

Mitochondrial ROS signalling requires uninterrupted electron flow and is lost during ageing in flies

Mitochondrial ROS signalling requires uninterrupted electron flow and is lost during ageing in flies

Oxidative Stress and Endoplasmic Reticulum Stress in Rare Respiratory Diseases

ROS signalling requires uninterrupted electron flow and is lost during ageing in flies

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