Mitochondrial autophagy promotes healthy aging

Shaik, Anjumara; Schiavi, Alfonso; Ventura, Natascia

doi:10.1080/15384101.2016.1181876

Cited by 15 publications

(8 citation statements)

References 7 publications

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“…Thus, reduced germ-cell proliferation during larval development, a critical stage for the specification of Mit mutants' longevity [36,63], may be either associated with or causally involved in lifespan extension in response to mitochondrial stress. In support of a causal connection between reduced germ-cell proliferation and lifespan extension is the number of mitotic and meiotic genes required for isp-1 mutants' longevity [23] and the tight crosstalk between cell proliferation and autophagy that could in turn modulate lifespan in response to mitochondrial stress [64][65][66][67]. Our data with the germline-less mutants and tissue-specific RNAi revealed a complex crosstalk between soma and the germline in the specification of isp-1 longevity, thus opening the interesting possibility for a role of mitotic and meiotic regulatory genes on somatic maintenance and lifespan independent of their classical role in cell cycle regulation.…”

Section: Discussionmentioning

confidence: 99%

BRCA 1 and BARD 1 mediate apoptotic resistance but not longevity upon mitochondrial stress in Caenorhabditis elegans

et al. 2018

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Interventions that promote healthy aging are typically associated with increased stress resistance. Paradoxically, reducing the activity of core biological processes such as mitochondrial or insulin metabolism promotes the expression of adaptive responses, which in turn increase animal longevity and resistance to stress. In this study, we investigated the relation between the extended Caenorhabditis elegans lifespan elicited by reduction in mitochondrial functionality and resistance to genotoxic stress. We find that reducing mitochondrial activity during development confers germline resistance to DNA damage‐induced cell cycle arrest and apoptosis in a cell‐non‐autonomous manner. We identified the C. elegans homologs of the BRCA1/BARD1 tumor suppressor genes, brc‐1/brd‐1, as mediators of the anti‐apoptotic effect but dispensable for lifespan extension upon mitochondrial stress. Unexpectedly, while reduced mitochondrial activity only in the soma was not sufficient to promote longevity, its reduction only in the germline or in germline‐less strains still prolonged lifespan. Thus, in animals with partial reduction in mitochondrial functionality, the mechanisms activated during development to safeguard the germline against genotoxic stress are uncoupled from those required for somatic robustness and animal longevity.

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Section: Discussionmentioning

confidence: 99%

BRCA 1 and BARD 1 mediate apoptotic resistance but not longevity upon mitochondrial stress in Caenorhabditis elegans

et al. 2018

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“…Therefore, fission is important for keeping mitochondrial quality and integrity. The level of both autophagy and mitophagy decline with aging, which results in an accumulation of dysfunctional mitochondria, advanced oxidative stress, and increased cell apoptosis. Dysfunctional mitochondrial accumulation occurs in all tissues during aging, including skeletal muscle, liver, and brain.…”

Section: Mitochondrial Anomalies With Agingmentioning

confidence: 99%

Mitochondrial dysfunction in neurodegenerative diseases and the potential countermeasure

et al. 2019

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Summary Mitochondria not only supply the energy for cell function, but also take part in cell signaling. This review describes the dysfunctions of mitochondria in aging and neurodegenerative diseases, and the signaling pathways leading to mitochondrial biogenesis (including PGC‐1 family proteins, SIRT1, AMPK) and mitophagy (parkin‐Pink1 pathway). Understanding the regulation of these mitochondrial pathways may be beneficial in finding pharmacological approaches or lifestyle changes (caloric restrict or exercise) to modulate mitochondrial biogenesis and/or to activate mitophagy for the removal of damaged mitochondria, thus reducing the onset and/or severity of neurodegenerative diseases.

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“…7 , top left). This function can be induced by various cellular stresses such as limited nutrients [106] , an accumulation of damaged proteins (aggrephagy) [107] , dysfunctional/defective mitochondria (mitophagy) [108] , [109] , and finally also by invading pathogens (xenophagy) [110] . Until now, at least 36 genes are known (Atg1-36, Atg for “autophagy-related protein”) which are involved in this still poorly understood process.…”

Section: Proteostasis Maintenance Systemsmentioning

confidence: 99%

Proteostasis, oxidative stress and aging

et al. 2017

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The production of reactive species is an inevitable by-product of metabolism and thus, life itself. Since reactive species are able to damage cellular structures, especially proteins, as the most abundant macromolecule of mammalian cells, systems are necessary which regulate and preserve a functional cellular protein pool, in a process termed “proteostasis”. Not only the mammalian protein pool is subject of a constant turnover, organelles are also degraded and rebuild. The most important systems for these removal processes are the “ubiquitin-proteasomal system” (UPS), the central proteolytic machinery of mammalian cells, mainly responsible for proteostasis, as well as the “autophagy-lysosomal system”, which mediates the turnover of organelles and large aggregates.Many age-related pathologies and the aging process itself are accompanied by a dysregulation of UPS, autophagy and the cross-talk between both systems. This review will describe the sources and effects of oxidative stress, preservation of cellular protein- and organelle-homeostasis and the effects of aging on proteostasis in mammalian cells.

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Mitochondrial autophagy promotes healthy aging

Cited by 15 publications

References 7 publications

BRCA 1 and BARD 1 mediate apoptotic resistance but not longevity upon mitochondrial stress in Caenorhabditis elegans

BRCA 1 and BARD 1 mediate apoptotic resistance but not longevity upon mitochondrial stress in Caenorhabditis elegans

Mitochondrial dysfunction in neurodegenerative diseases and the potential countermeasure

Proteostasis, oxidative stress and aging

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