Complex-I-ty in aging

Hur, Jae H.; Stork, Devon; Walker, David W.

doi:10.1007/s10863-014-9553-0

Cited by 23 publications

(17 citation statements)

References 57 publications

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“…Similar lifespan extension was conferred by Ndx, the NDH2 from Ciona intestinalis (Gospodaryov et al, 2014). It was initially assumed that lifespan extension by NDH2 is due to a) a decrease in NADH/NAD + ratio (Stefanatos and Sanz, 2011;Scialò et al, 2013;Hur et al, 2014) or b) a decrease in ROS production by complex I (Scialò et al, 2013). It was recently shown that mitochondria of Ndi1p-expressing cells produced more ROS (Scialò et al, 2016).…”

Section: Ndh2 As a Tool To Study Ageingmentioning

confidence: 93%

Alternative NAD(P)H dehydrogenase and alternative oxidase: Proposed physiological roles in animals

McDonald

Gospodaryov

2019

Mitochondrion

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The electron transport systems in mitochondria of many organisms contain alternative respiratory enzymes distinct from those of the canonical respiratory system depicted in textbooks. Two of these enzymes, the alternative NADH dehydrogenase and the alternative oxidase, were of interest to a limited circle of researchers until they were envisioned as gene therapy tools for mitochondrial disease treatment. Recently, these enzymes were discovered in several animals. Here, we analyse the functioning of alternative NADH dehydrogenases and oxidases in different organisms. We propose that both enzymes ensure bioenergetic and metabolic flexibility during environmental transitions or other conditions which may compromise the operation of the canonical respiratory system.

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Section: Ndh2 As a Tool To Study Ageingmentioning

confidence: 93%

Alternative NAD(P)H dehydrogenase and alternative oxidase: Proposed physiological roles in animals

McDonald

Gospodaryov

2019

Mitochondrion

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“…This may make PCD pathways particularly vulnerable to maladaptive signals during aging. Third, the important role of the mitochondria and ROS in PCD is likely a factor, because mitochondria appear to be particularly susceptible to damage and malfunction during aging across species (Bernhardt et al, 2014; Hur et al, 2014; Wallace, 2010). …”

Section: Why Is Pcd Mis-regulated During Aging?mentioning

confidence: 99%

Programmed cell death in aging

Tower

2015

Ageing Research Reviews

313

208

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Programmed cell death (PCD) pathways, including apoptosis and regulated necrosis, are required for normal cell turnover and tissue homeostasis. Mis-regulation of PCD is increasingly implicated in aging and aging-related disease. During aging the cell turnover rate declines for several highly-mitotic tissues. Aging-associated disruptions in systemic and inter-cell signaling combined with cell-autonomous damage and mitochondrial malfunction result in increased PCD in some cell types, and decreased PCD in other cell types. Increased PCD during aging is implicated in immune system decline, skeletal muscle wasting (sarcopenia), loss of cells in the heart, and neurodegenerative disease. In contrast, cancer cells and senescent cells are resistant to PCD, enabling them to increase in abundance during aging. PCD pathways limit life span in fungi, but whether PCD pathways normally limit adult metazoan life span is not yet clear. PCD is regulated by a balance of negative and positive factors, including the mitochondria, which are particularly subject to aging-associated malfunction.

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“…In both Drosophila and C. elegans , RNAi inhibition of certain genes encoding ETC components can increase life span [7, 313–315]. This result was initially interpreted to suggest that life span increase might be due to decreased metabolic activity.…”

Section: The Mitochondrial Stress Response and Unfolded Protein Respomentioning

confidence: 99%

Mitochondrial maintenance failure in aging and role of sexual dimorphism

Tower¹

2015

Archives of Biochemistry and Biophysics

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Gene expression changes during aging are partly conserved across species, and suggest that oxidative stress, inflammation and proteotoxicity result from mitochondrial malfunction and abnormal mitochondrial-nuclear signaling. Mitochondrial maintenance failure may result from trade-offs between mitochondrial turnover versus growth and reproduction, sexual antagonistic pleiotropy and genetic conflicts resulting from uni-parental mitochondrial transmission, as well as mitochondrial and nuclear mutations and loss of epigenetic regulation. Aging phenotypes and interventions are often sex-specific, indicating that both male and female sexual differentiation promote mitochondrial failure and aging. Studies in mammals and invertebrates implicate autophagy, apoptosis, AKT, PARP, p53 and FOXO in mediating sex-specific differences in stress resistance and aging. The data support a model where the genes Sxl in Drosophila, sdc-2 in C. elegans, and Xist in mammals regulate mitochondrial maintenance across generations and in aging. Several interventions that increase life span cause a mitochondrial unfolded protein response (UPRmt), and UPRmt is also observed during normal aging, indicating hormesis. The UPRmt may increase life span by stimulating mitochondrial turnover through autophagy, and/or by inhibiting the production of hormones and toxic metabolites. The data suggest that metazoan life span interventions may act through a common hormesis mechanism involving liver UPRmt, mitochondrial maintenance and sexual differentiation.

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Complex-I-ty in aging

Cited by 23 publications

References 57 publications

Alternative NAD(P)H dehydrogenase and alternative oxidase: Proposed physiological roles in animals

Alternative NAD(P)H dehydrogenase and alternative oxidase: Proposed physiological roles in animals

Programmed cell death in aging

Mitochondrial maintenance failure in aging and role of sexual dimorphism

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