Iron-starvation-induced mitophagy mediates lifespan extension upon mitochondrial stress in C.elegans
Open accessAbstract
Frataxin is a nuclear-encoded mitochondrial protein involved in the biogenesis of Fe-S-cluster-containing proteins and consequently in the functionality of the mitochondrial respiratory chain. Similar to other proteins that regulate mitochondrial respiration, severe frataxin deficiency leads to pathology in humans--Friedreich's ataxia, a life-threatening neurodegenerative disorder--and to developmental arrest in the nematode C. elegans. Interestingly, partial frataxin depletion extends C. elegans lifespan, and a similar anti-aging effect is prompted by reduced expression of other mitochondrial regulatory proteins from yeast to mammals. The beneficial adaptive responses to mild mitochondrial stress are still largely unknown and, if characterized, may suggest novel potential targets for the treatment of human mitochondria-associated, age-related disorders. Here we identify mitochondrial autophagy as an evolutionarily conserved response to frataxin silencing, and show for the first time that, similar to mammals, mitophagy is activated in C. elegans in response to mitochondrial stress in a pdr-1/Parkin-, pink-1/Pink-, and dct-1/Bnip3-dependent manner. The induction of mitophagy is part of a hypoxia-like, iron starvation response triggered upon frataxin depletion and causally involved in animal lifespan extension. We also identify non-overlapping hif-1 upstream (HIF-1-prolyl-hydroxylase) and downstream (globins) regulatory genes mediating lifespan extension upon frataxin and iron depletion. Our findings indicate that mitophagy induction is part of an adaptive iron starvation response induced as a protective mechanism against mitochondrial stress, thus suggesting novel potential therapeutic strategies for the treatment of mitochondrial-associated, age-related disorders.
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Mild mitochondrial dysfunction promotes longevity.
“many data indicate indeed that a mild mitochondrial dysfunction actually promotes longevity (5,6).”
From Human Aging and Longevity Are Characterized by High Levels of Mitokines (2019) · cites this paper as [6]
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- Authors
- Schiavi, A., Maglioni, S., Palikaras, K., Shaik, A., Strappazzon, F., Brinkmann, V., Torgovnick, A., Castelein, N., De Henau, S., Braeckman, B. P., Cecconi, F., Tavernarakis, N., & Ventura, N.
- Affiliations
- University of Rome Tor Vergata (IT)
- Leibniz Institute of Environmental Medicine (DE)
- Foundation for Research and Technology Hellas (GR)
- Ghent University (BE)
- University of Crete (GR)
- Corresponding author
- Ventura, Natascia
- ORCID
- Venue
- Current Biology
- Publisher
- Elsevier BV
- Published
- 2015-07
- Volume
- 25
- Issue
- 14
- Pages
- 1810-1822
- ISSN
- 0960-9822 (ISSN-L)
- OpenAlex
- W1919124805
- Cited by
- 209
- References
- 56
- Citations by year
- 2026: 8 · 2025: 11 · 2024: 17 · 2023: 9 · 2022: 22 · 2021: 18 · 2020: 32 · 2019: 24 · 2018: 23 · 2017: 21 · 2016: 21 · 2015: 2
- FWCI
- 8.95
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Current Biology (publishedVersion)
- PubMed (publishedVersion)
- Ghent University Academic Bibliography (Ghent University) (submittedVersion)
- Cineca Institutional Research Information System (Tor Vergata University) (submittedVersion)
- Funders
- National Institutes of Health (P40OD010440)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Keywords
- frataxin, mitophagy, mitochondrial stress, iron starvation, lifespan extension, Friedreich's ataxia, globin, mitochondrial biogenesis, aging, Caenorhabditis elegans
- MeSH terms
- Iron Deficiencies, Frataxin, Anaerobiosis, Animals, Fasting, Longevity, Caenorhabditis elegans, Caenorhabditis elegans Proteins, Iron-Binding Proteins, Mitophagy
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