ArticleAging cell2017
In vivo imaging reveals mitophagy independence in the maintenance of axonal mitochondria during normal aging.
Article in Aging cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
22 citing papers in PubMed, 34 citations in OpenAlex.
- Targeting Mitochondria in Aging-Related Diseases: Therapeutic Potential and Obstacles.MedComm · 2026Review
- Impacts of mitochondrial dysfunction on axonal microtubule bundles as a potential mechanism of neurodegeneration.Frontiers in neuroscience · 2025Review
- COPI-regulated mitochondria-ER contact site formation maintains axonal integrity.Cell reports · 2023Article
- Article
- Light-activated mitochondrial fission through optogenetic control of mitochondria-lysosome contacts.Nature communications · 2022Article
- Are mitophagy enhancers therapeutic targets for Alzheimer's disease?Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2022Review
- Mitochondrial fusion regulates proliferation and differentiation in the type II neuroblast lineage in Drosophila.PLoS genetics · 2022Article
- CHMP2B regulates TDP-43 phosphorylation and cytotoxicity independent of autophagy via CK1.The Journal of cell biology · 2022Article
- A Dual-Labeling Probe for Super-Resolution Imaging to Detect Mitochondrial Reactive Sulfur Species in Live Cells.Frontiers in pharmacology · 2022Article
- The NRF2-Dependent Transcriptional Regulation of Antioxidant Defense Pathways: Relevance for Cell Type-Specific Vulnerability to Neurodegeneration and Therapeutic Intervention.Antioxidants (Basel, Switzerland) · 2021Review
- Mitochondrial fission, integrity and completion of mitophagy require separable functions of Vps13D in Drosophila neurons.PLoS genetics · 2021Article
- A Perspective on Accelerated Aging Caused by the Genetic Deficiency of the Metabolic Protein, OPA1.Frontiers in neurology · 2021Article
- Mitochondrial Behavior in Axon Degeneration and Regeneration.Frontiers in aging neuroscience · 2021Review
- Effects of Aging on Expression ofAnimals : an open access journal from MDPI · 2020Article
- SUMOylation in α-Synuclein Homeostasis and Pathology.Frontiers in aging neuroscience · 2020Review
- Endoplasmic reticulum mediates mitochondrial transfer within the osteocyte dendritic network.Science advances · 2019Article
- Organelle aging: Lessons from model organisms.Journal of genetics and genomics = Yi chuan xue bao · 2019Review
- Rapid depletion of ESCRT protein Vps4 underlies injury-induced autophagic impediment and Wallerian degeneration.Science advances · 2019Article
- Endogenous formaldehyde is a memory-related molecule in mice and humans.Communications biology · 2019Article
- Temporal Control of Axonal Transport: The Extreme Case of Organismal Ageing.Frontiers in cellular neuroscience · 2019Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitophagy is thought to be a critical mitochondrial quality control mechanism in neurons and has been extensively studied in neurological disorders such as Parkinson's disease. However, little is known about how mitochondria are maintained in the lengthy neuronal axons in the context of physiological aging. Here, we utilized the unique Drosophila wing nerve model and in vivo imaging to rigorously profile changes in axonal mitochondria during aging. We revealed that mitochondria became fragmented and accumulated in aged axons. However, lack of Pink1 or Parkin did not lead to the accumulation of axonal mitochondria or axonal degeneration. Further, unlike in in vitro cultured neurons, we found that mitophagy rarely occurred in intact axons in vivo, even in aged animals. Furthermore, blocking overall mitophagy by knockdown of the core autophagy genes Atg12 or Atg17 had little effect on the turnover of axonal mitochondria or axonal integrity, suggesting that mitophagy is not required for axonal maintenance; this is regardless of whether the mitophagy is PINK1-Parkin dependent or independent. In contrast, downregulation of mitochondrial fission-fusion genes caused age-dependent axonal degeneration. Moreover, Opa1 expression in the fly head was significantly decreased with age, which may underlie the accumulation of fragmented mitochondria in aged axons. Finally, we showed that adult-onset, neuronal downregulation of the fission-fusion, but not mitophagy genes, dramatically accelerated features of aging. We propose that axonal mitochondria are maintained independently of mitophagy and that mitophagy-independent mechanisms such as fission-fusion may be central to the maintenance of axonal mitochondria and neural integrity during normal aging.
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Registered trials
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