ArticlePloS one2019
Overexpression of pink1 or parkin in indirect flight muscles promotes mitochondrial proteostasis and extends lifespan in Drosophila melanogaster.
Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 36 citations in OpenAlex.
- FAM162A Is a Key Regulator of Mitochondrial Structure, Dynamics, and Bioenergetics, Driving Cellular Protection and Longevity.Aging cell · 2026Article
- Parkin overexpression attenuates muscle atrophy and improves mitochondrial bioenergetics but not histological features of Duchenne muscular dystrophy in mice.Scientific reports · 2026Article
- Parkin overexpression modulates gut-microbiota composition during aging inFrontiers in microbiology · 2025Article
- Targeting ATAD3A Phosphorylation Mediated by TBK1 Ameliorates Senescence-Associated Pathologies.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Article
- Interactions of mitochondrial and skeletal muscle biology in mitochondrial myopathy.The Biochemical journal · 2023Review
- The Small-Molecule Enhancers of Autophagy AUTEN-67 and -99 Delay Ageing inInternational journal of molecular sciences · 2023Article
- Role of muscle FOXO gene in exercise against the skeletal muscle and cardiac age-related defects and mortality caused by high-salt intake in Drosophila.Genes & nutrition · 2023Article
- Senolytic and senomorphic secondary metabolites as therapeutic agents inFrontiers in neurology · 2023Review
- Markers and mechanisms of death inFrontiers in aging · 2023Article
- PINK1 overexpression prevents forskolin-induced tau hyperphosphorylation and oxidative stress in a rat model of Alzheimer's disease.Acta pharmacologica Sinica · 2022Article
- Reversible mitophagy drives metabolic suppression in diapausing beetles.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Ubiquitin Ligases in Longevity and Aging Skeletal Muscle.International journal of molecular sciences · 2022Review
- Role of the mtDNA Mutations and Mitophagy in Inflammaging.International journal of molecular sciences · 2022Review
- Artemisinin Alleviates Cerebral Ischemia/Reperfusion-Induced Oxidative Damage via Regulating PHB2-Mediated Autophagy in the Human Neuroblastoma SH-SY5Y Cell Line.Oxidative medicine and cellular longevity · 2022Article
- Gene Therapeutic Approaches for the Treatment of Mitochondrial Dysfunction in Parkinson's Disease.Genes · 2021Review
- Mitophagy and Oxidative Stress: The Role of Aging.Antioxidants (Basel, Switzerland) · 2021Review
- The connection between the dynamic remodeling of the mitochondrial network and the regulation of muscle mass.Cellular and molecular life sciences : CMLS · 2021Review
- Proteostasis-associated aging: lessons from a Drosophila model.Genes & genomics · 2021Review
- The Interplay between Mitochondrial Morphology and Myomitokines in Aging Sarcopenia.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dysfunctional mitochondria have been implicated in aging and age-related disorders such as Parkinson's diseases (PD). We previously showed that pink1 and parkin, two familial PD genes, function in a linear pathway to maintain mitochondrial integrity and function. Studies of mammalian cell lines also suggest that these genes regulate mitochondrial autophagy(mitophagy). Overexpressing Parkin promotes proteostasis and function of aged muscles both in fruit flies and mice, and recent studies also indicated that mitochondrial ubiquitination are accumulated in aged muscles. However, the underlying mechanisms for pink1 and parkin mediated mitophagy on longevity is not fully understood. Here, we found that mitochondrial ubiquitination increased in indirect flight muscles (IFMs) in an age-dependent manner. Overexpression of pink1 or parkin in IFMs can abolish mitochondrial ubiquitination, restore ATP level and extend lifespan, while blocking autophagy via ATG1 knock-down suppress these effects in aged IFMs. Taken together, these results show that pink1/parkin promotes mitophagy of mitochondrial ubiquitination in aged muscles and extend lifespan in an Atg1-dependent manner. Our study provides physiological evidence that mitophagy of mitochondrial ubiquitination mediated by PINK1/ Parkin is crucial for muscle function and highlights the role of mitophagy in the pathogenesis of chronic diseases like PD.
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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.