ArticleThe Journal of biological chemistry2020
The short variant of optic atrophy 1 (OPA1) improves cell survival under oxidative stress.
Article in The Journal of biological chemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 63 citations in OpenAlex.
- Herpes simplex virus 1 subverts the mitochondrial network to support the infection: A lesson on mitochondrial versatility.bioRxiv : the preprint server for biology · 2026Article
- Discovery of PHB1 as a Novel Candidate Gene in Dominant Optic Atrophy.Clinical genetics · 2026Article
- Succinate and lactate produced as conserved biomarkers through chronic and transient substrate-level phosphorylation: from microorganisms to cancer.Journal of bioenergetics and biomembranes · 2026Review
- Failure of efficient cardiac proteostatic adaptations to chronic cAMP-stress is associated with accelerated heart aging.GeroScience · 2026Article
- FAM162A Is a Key Regulator of Mitochondrial Structure, Dynamics, and Bioenergetics, Driving Cellular Protection and Longevity.Aging cell · 2026Article
- Cancer cells surviving cisplatin chemotherapy increase stress-induced OMA1 activity and mitochondrial fragmentation.Scientific reports · 2026Article
- Integrated bioinformatic and in vivo analysis confirms the cardioprotective role of OPA1.BMC cardiovascular disorders · 2025Article
- Cancer cells surviving cisplatin chemotherapy increase stress-induced OMA1 activity and mitochondrial fragmentation.bioRxiv : the preprint server for biology · 2025Article
- Disruption of Mitochondrial Quality Control in Inherited Metabolic Disorders.Molecular neurobiology · 2025Review
- Mitochondria-derived vesicles: A promising and potential target for tumour therapy.Clinical and translational medicine · 2025Review
- Tetrahydrobenzimidazole TMQ0153 targets OPA1 and restores drug sensitivity in AML via ROS-induced mitochondrial metabolic reprogramming.Journal of experimental & clinical cancer research : CR · 2025Article
- Disruption of mitochondrial homeostasis and permeability transition pore opening in OPA1 iPSC-derived retinal ganglion cells.Acta neuropathologica communications · 2025Article
- Compound heterozygous mutation of AFG3L2 causes autosomal recessive spinocerebellar ataxia through mitochondrial impairment and MICU1 mediated CaScience China. Life sciences · 2025Article
- Long-term mitochondrial and metabolic impairment in lymphocytes of subjects who recovered after severe COVID-19.Cell biology and toxicology · 2025Article
- Mitochondrial dynamics at the intersection of macrophage polarization and metabolism.Frontiers in immunology · 2025Review
- The Novel Anticancer Aryl-Ureido Fatty Acid CTU Increases Reactive Oxygen Species Production That Impairs Mitochondrial Fusion Mechanisms and Promotes MDA-MB-231 Cell Death.International journal of molecular sciences · 2024Article
- Infection-induced peripheral mitochondria fission drives ER encapsulations and inter-mitochondria contacts that rescue bioenergetics.Nature communications · 2024Article
- OPA1 promotes ferroptosis by augmenting mitochondrial ROS and suppressing an integrated stress response.Molecular cell · 2024Article
- OMA1-Mediated Mitochondrial Dynamics Balance Organellar Homeostasis Upstream of Cellular Stress Responses.International journal of molecular sciences · 2024Review
- Attenuating mitochondrial dysfunction and morphological disruption with PT320 delays dopamine degeneration in MitoPark mice.Journal of biomedical science · 2024Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Optic atrophy 1 (OPA1) is a dynamin protein that mediates mitochondrial fusion at the inner membrane. OPA1 is also necessary for maintaining the cristae and thus essential for supporting cellular energetics. OPA1 exists as membrane-anchored long form (L-OPA1) and short form (S-OPA1) that lacks the transmembrane region and is generated by cleavage of L-OPA1. Mitochondrial dysfunction and cellular stresses activate the inner membrane-associated zinc metallopeptidase OMA1 that cleaves L-OPA1, causing S-OPA1 accumulation. The prevailing notion has been that L-OPA1 is the functional form, whereas S-OPA1 is an inactive cleavage product in mammals, and that stress-induced OPA1 cleavage causes mitochondrial fragmentation and sensitizes cells to death. However, S-OPA1 contains all functional domains of dynamin proteins, suggesting that it has a physiological role. Indeed, we recently demonstrated that S-OPA1 can maintain cristae and energetics through its GTPase activity, despite lacking fusion activity. Here, applying oxidant insult that induces OPA1 cleavage, we show that cells unable to generate S-OPA1 are more sensitive to this stress under obligatory respiratory conditions, leading to necrotic death. These findings indicate that L-OPA1 and S-OPA1 differ in maintaining mitochondrial function. Mechanistically, we found that cells that exclusively express L-OPA1 generate more superoxide and are more sensitive to Ca
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