ArticleCell death & disease2016
PINK1 and Parkin cooperatively protect neurons against constitutively active TRP channel-induced retinal degeneration in Drosophila.
Article in Cell death & disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 29 citations in OpenAlex.
- Pharmacological restoration of impaired autophagy in retinal ganglion cells prevents abnormal mitochondrial accumulation and glaucomatous neurodegeneration.Molecular neurodegeneration · 2026Article
- Perturbation of Anion/Cation Transport Leads to Apical Panicle Abortion in Rice by Disrupting CaPlant biotechnology journal · 2026Article
- Distinct roles of clustered MicroRNAs miR-286 and miR-6 in JNK activation critical to apoptosis-induced proliferation in Drosophila.Cellular and molecular life sciences : CMLS · 2025Article
- Electroacupuncture alleviates damage to myopic RGCs probably through lncRNA-XR_002789763.1-mediated mitophagy.Chinese medicine · 2025Article
- Retinal G-protein-coupled receptor deletion exacerbates AMD-like changes via the PINK1-parkin pathway under oxidative stress.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- PINK1-PRKN mediated mitophagy: differences betweenAutophagy · 2023Review
- MFN1 augmentation prevents retinal degeneration in a Charcot-Marie-Tooth type 2A mouse model.iScience · 2023Article
- Neuronal autophagy and mitophagy in Parkinson's disease.Molecular aspects of medicine · 2021Review
- Deciphering the dual role and prognostic potential of PINK1 across cancer types.Neural regeneration research · 2021Article
- Proteostasis-associated aging: lessons from a Drosophila model.Genes & genomics · 2021Review
- PINK1: Multiple mechanisms of neuroprotection.International review of movement disorders · 2021Article
- PINK1/PARKIN signalling in neurodegeneration and neuroinflammation.Acta neuropathologica communications · 2020Review
- Article
- Increased Levels of cAMP by the Calcium-Dependent Activation of Soluble Adenylyl Cyclase inCells · 2019Article
- dTBC1D7 regulates systemic growth independently of TSC through insulin signaling.The Journal of cell biology · 2018Article
- The role of CaDisease models & mechanisms · 2017Review
- Epigenetic Treatment of Neurodegenerative Ophthalmic Disorders: An Eye Toward the Future.BioResearch open access · 2017Review
- Cytochrome b5 protects photoreceptors from light stress-induced lipid peroxidation and retinal degeneration.NPJ aging and mechanisms of disease · 2017Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Calcium has an important role in regulating numerous cellular activities. However, extremely high levels of intracellular calcium can lead to neurotoxicity, a process commonly associated with degenerative diseases. Despite the clear role of calcium cytotoxicity in mediating neuronal cell death in this context, the pathological mechanisms remain controversial. We used a well-established Drosophila model of retinal degeneration, which involves the constitutively active TRP(P365) channels, to study calcium-induced neurotoxicity. We found that the disruption of mitochondrial function was associated with the degenerative process. Further, increasing autophagy flux prevented cell death in Trp(P365) mutant flies, and this depended on the PINK1/Parkin pathway. In addition, the retinal degeneration process was also suppressed by the coexpression of PINK1 and Parkin. Our results provide genetic evidence that mitochondrial dysfunction has a key role in the pathology of cellular calcium neurotoxicity. In addition, the results demonstrated that maintaining mitochondrial homeostasis via PINK1/Parkin-dependent mitochondrial quality control can potentially alleviate cell death in a wide range of neurodegenerative diseases.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.