ArticleCell death & disease2023
Coupling of autophagy and the mitochondrial intrinsic apoptosis pathway modulates proteostasis and ageing in Caenorhabditis elegans.
Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 76 citations in OpenAlex.
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- Lysosomal control of proteostasis and reproductive capacity by conserved LMD-3 protein inScience advances · 2025Article
- Ferric Uptake Regulator Contributes toMicroorganisms · 2025Article
- Predictive and therapeutic value of the ferroptosis gene CISD1 in non?small cell lung cancer.Oncology letters · 2025Article
- Review
- The role of CISD1 reduction in macrophages in promoting COPD development through M1 polarization and mitochondrial dysfunction.European journal of medical research · 2024Article
- The neurotrophic factor MANF regulates autophagy and lysosome function to promote proteostasis inProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Cathelicidin boosts the antifungal activity of neutrophils and improves prognosis duringInfection and immunity · 2024Article
- Neurotrophic factor MANF regulates autophagy and lysosome function to promote proteostasis inbioRxiv : the preprint server for biology · 2024Article
- Editorial: Novel strategies to target cell death signaling in cancer and neurodegenerative diseases: new findings and mechanistic studies.Frontiers in cell and developmental biology · 2024Article
- Mitochondria in the Spotlight:Cells · 2023Review
- Caenorhabditis elegans for research on cancer hallmarks.Disease models & mechanisms · 2023Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondria preserve metabolic homeostasis and integrate stress signals, to trigger cytoprotective, or cell death pathways. Mitochondrial homeostasis and function decline with age. The mechanisms underlying the deterioration of mitochondrial homeostasis during ageing, or in age-associated pathologies, remain unclear. Here, we show that CISD-1, a mitochondrial iron-sulfur cluster binding protein, implicated in the pathogenesis of Wolfram neurodegenerative syndrome type 2, modulates longevity in the nematode Caenorhabditis elegans by engaging autophagy and the mitochondrial intrinsic apoptosis pathway. The anti-apoptotic protein CED-9 is the downstream effector that mediates CISD-1-dependent effects on proteostasis, neuronal integrity and lifespan. Moreover, intracellular iron abundance is critical for CISD-1 function, since mild iron supplementation is sufficient to decelerate ageing and partly ameliorate the disturbed mitochondrial bioenergetics and proteostasis of CISD-1 deficient animals. Our findings reveal that CISD-1 serves as a mechanistic link between autophagy and the apoptotic pathway in mitochondria to differentially modulate organismal proteostasis and ageing, and suggest novel approaches which could facilitate the treatment of Wolfram Syndrome or related diseases.
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