ArticleBritish journal of pharmacology2013
3-Nitropropionic acid induces autophagy by forming mitochondrial permeability transition pores rather than activating the mitochondrial fission pathway.
Article in British journal of pharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 60 citations in OpenAlex.
- Sensory decline in aging and neurodegeneration: A mitochondrial perspective.Pharmacological research · 2026Review
- Effects of nutrients and diet on mitochondrial dysfunction: An opportunity for therapeutic approaches in human disease.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2025Review
- Progress on 3-Nitropropionic Acid Derivatives.Biomolecules · 2025Review
- Mitochondrial quality control disorder in neurodegenerative disorders: Potential and advantages of traditional Chinese medicines.Journal of pharmaceutical analysis · 2025Review
- Short-term starvation activates AMPK and restores mitochondrial inorganic polyphosphate, but fails to reverse associated neuronal senescence.Aging cell · 2024Article
- Anandamide and WIN 55212-2 Afford Protection in Rat Brain Mitochondria in a Toxic Model Induced by 3-Nitropropionic Acid: an In Vitro Study.Molecular neurobiology · 2024Article
- Nanobodies as novel tools to monitor the mitochondrial fission factor Drp1.Life science alliance · 2024Article
- Mitophagy in intracerebral hemorrhage: a new target for therapeutic intervention.Neural regeneration research · 2024Review
- Mitochondrial inorganic polyphosphate is required to maintain proteostasis within the organelle.Frontiers in cell and developmental biology · 2024Article
- Toolkit for cellular studies of mammalian mitochondrial inorganic polyphosphate.Frontiers in cell and developmental biology · 2023Article
- A novel small molecule inhibitor of human Drp1.Scientific reports · 2022Article
- COVID-19 and neurodegeneration: The mitochondrial connection.Aging cell · 2022Article
- Enzymatic Depletion of Mitochondrial Inorganic Polyphosphate (polyP) Increases the Generation of Reactive Oxygen Species (ROS) and the Activity of the Pentose Phosphate Pathway (PPP) in Mammalian Cells.Antioxidants (Basel, Switzerland) · 2022Article
- Mitochondrial Inorganic Polyphosphate (polyP) Is a Potent Regulator of Mammalian Bioenergetics in SH-SY5Y Cells: A Proteomics and Metabolomics Study.Frontiers in cell and developmental biology · 2022Article
- Mitochondrial Abnormalities and Synaptic Damage in Huntington's Disease: a Focus on Defective Mitophagy and Mitochondria-Targeted Therapeutics.Molecular neurobiology · 2021Review
- ATP Synthase and Mitochondrial Bioenergetics Dysfunction in Alzheimer's Disease.International journal of molecular sciences · 2021Review
- Review
- Depletion of mitochondrial inorganic polyphosphate (polyP) in mammalian cells causes metabolic shift from oxidative phosphorylation to glycolysis.The Biochemical journal · 2021Article
- New insights into targeting mitochondria in ischemic injury.Apoptosis : an international journal on programmed cell death · 2021Review
- Inhibition of mitochondrial complex II in neuronal cells triggers unique pathways culminating in autophagy with implications for neurodegeneration.Scientific reports · 2021Article
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4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeHuntington's disease is a neurodegenerative process associated with mitochondrial alterations. Inhibitors of the electron-transport channel complex II, such as 3-nitropropionic acid (3NP), are used to study the molecular and cellular pathways involved in this disease. We studied the effect of 3NP on mitochondrial morphology and its involvement in macrophagy. EXPERIMENTAL APPROACH: Pharmacological and biochemical methods were used to characterize the effects of 3NP on autophagy and mitochondrial morphology. SH-SY5Y cells were transfected with GFP-LC3, GFP-Drp1 or GFP-Bax to ascertain their role and intracellular localization after 3NP treatment using confocal microscopy. KEY
resultsUntreated SH-SY5Y cells presented a long, tubular and filamentous net of mitochondria. After 3NP (5 mM) treatment, mitochondria became shorter and rounder. 3NP induced formation of mitochondrial permeability transition pores, both in cell cultures and in isolated liver mitochondria, and this process was inhibited by cyclosporin A. Participation of the mitochondrial fission pathway was excluded because 3NP did not induce translocation of the dynamin-related protein 1 (Drp1) to the mitochondria. The Drp1 inhibitor Mdivi-1 did not affect the observed changes in mitochondrial morphology. Finally, scavengers of reactive oxygen species failed to prevent mitochondrial alterations, while cyclosporin A, but not Mdivi-1, prevented the generation of ROS. CONCLUSIONS AND IMPLICATIONS: There was a direct correlation between formation of mitochondrial permeability transition pores and autophagy induced by 3NP treatment. Activation of autophagy preceded the apoptotic process and was mediated, at least partly, by formation of reactive oxygen species and mitochondrial permeability transition pores.
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