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Mitophagy of damaged mitochondria occurs locally in distal neuronal axons and requires PINK1 and Parkin
Open accessAbstract
To minimize oxidative damage to the cell, malfunctioning mitochondria need to be removed by mitophagy. In neuronal axons, mitochondrial damage may occur in distal regions, far from the soma where most lysosomal degradation is thought to occur. In this paper, we report that PINK1 and Parkin, two Parkinson’s disease–associated proteins, mediate local mitophagy of dysfunctional mitochondria in neuronal axons. To reduce cytotoxicity and mimic physiological levels of mitochondrial damage, we selectively damaged a subset of mitochondria in hippocampal axons. Parkin was rapidly recruited to damaged mitochondria in axons followed by formation of LC3-positive autophagosomes and LAMP1-positive lysosomes. In PINK1−/− axons, damaged mitochondria did not accumulate Parkin and failed to be engulfed in autophagosomes. Similarly, initiation of mitophagy was blocked in Parkin−/− axons. Our findings demonstrate that the PINK1–Parkin-mediated pathway is required for local mitophagy in distal axons in response to focal damage. Local mitophagy likely provides rapid neuroprotection against oxidative stress without a requirement for retrograde transport to the soma.
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“Axonal autophagy is dependent on specialized enzymatic apparatuses, including the PINK1-PRKN complex for localized mitophagy [24], KIF1A/UNC-104 for autophagosome formation at the synapse [22,25], and the HTT-HAP1 complex and MAPK8IP1/JIP1 for retrograde transport of autophagosomes [23,26].”
From Autophagy and ALS: mechanistic insights and therapeutic implications (2022) · cites this paper as [22]
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Cites
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“Although PINK1/Parkin-mediated mitophagy was shown to occur in axons of cultured neurons (Ashrafi et al., 2014; Bingol et al., 2014), there is still debate about whether these mechanisms take place in neurons in vivo.”
BackgroundEstimating the Binding and Unbinding Rate of Motor Protein from Mitochondrial Motion
Chen, X., Li, M., Chen, T., Du, S., & Li, Y. (2020) · IEEE Global Conference on Life Sciences and Technologies (LifeTech) · doi:10.1109/lifetech48969.2020.1570618909 · Cited by 1
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Drosophila HS dendrites are resilient to adult-onset deficits in mitochondrial dynamicsPreprint
Wang, H. Q., Fortson, D. G., Burton, E. D., Whitbeck, H. S., Robles, B. M., Bortey, L., Adler, A. J., Kalai, J. I., Napoleone, G., & Barnhart, E. L. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.11.07.687201
“…via piecemeal degradation of mitochondrial proteins and mitochondria-derived vesicles and/or via local mitophagy or macroautophagy followed by retrograde trafficking of autophagosomes (Ashrafi et al., 2014; Cason et al., 2022; Goldsmith et al., 2022; Maday et al., 2012; Misgeld and Schwarz, 2017).”
Mu, N., Zhang, T., Zhu, Y., Lu, B., Zheng, Q., & Duan, J. (2024) · Figshare · doi:10.6084/m9.figshare.26584233
Agujetas, V. R., Barbero-Camps, E., de Dios, C., Podlesniy, P., Abadin, X., Morales, A., Marı́, M., Trullás, R., & Colell, A. (2021) · Figshare · doi:10.6084/m9.figshare.14183579
Wisner, S. R., Stein, C., Smith, E. E., Hoon, M., & Drerup, C. M. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2025.12.26.696432
“This mechanism has been engaged previously through the use of mitochondria depolarizing agents such as Antimycin A, CCCP and Killer Red 9,37,56 .”
Regulation of neuronal microtubule-based transport by polyglutamylation
Bodakuntla, S. (2019) · theses.fr (ABES) · doi:10.70675/25a5f130z3b63z4663zb3aez400da5d97e80
Contrôle de la mitophagie dans la maladie de Parkinson : Dialogue fonctionnel entre XBP1 et PINK1
Manaa, W. E. (2019) · theses.fr (ABES) · doi:10.70675/3428bd72z68cdz42f6za6d1z35ce71263711
Miressi, F. (2020) · theses.fr (ABES) · doi:10.70675/ccae6ea0ze325z4808zab41z83e3b4a1a7bf
Lanfranchi, M. (2021) · theses.fr (ABES) · doi:10.70675/247335b1zba7fz4005zafbdzdc43c088d75f
The Interaction Between Miro and TRAK is not Required for Bulk Mitochondrial TraffickingPreprint
Covill‐Cooke, C., Owens, M., Prokop, A., & Kornmann, B. (2026) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2026.05.01.722185
“…trafficking field since its formulation in the 2000s, and underpins most – if not all – of the work on the regulation of mitochondrial trafficking in different cellular contexts (Macaskill et al., 2009; Wang and Schwarz, 2009; Wang et al., 2011; Ashrafi et al., 2014; McKenna et al., 2025).”
Wang, M., Zhang, Z., Sha, Z., Zhang, F., & Bao, K. (2026) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2026.1808059
“This blocks dynein-dependent retrograde transport and “traps” damaged mitochondria in place (Ashrafi et al., 2014; Ge et al., 2020).”
Local translation of endosome-associated lc3b mRNA in axons contributes to endosomal clearance
Pappacena, F., Caterino, C., de Pretis, S., Sironi, C., Esposito, A., Cesare, G., Bruni, M., & Cioni, J.-M. (2026) · EMBO Reports · doi:10.1038/s44319-026-00867-5
The role of impaired mitochondrial function in neurological manifestations of mitochondrial diseases
Brister, D., Zarate-Mendez, M., Hathazi, D., & Horváth, R. (2026) · Mammalian Genome · doi:10.1007/s00335-026-10278-5
“In addition, mitophagy of damaged mitochondria can also occur locally (Ashrafi et al. 2014), a critical function given the high exposure of synaptic mitochondria to reactive oxygen species, excitotoxic damage and other stressors (Völgyi et al. 2015).”
Zhang, Z.-Y., Qin, B., Shi-zhou, W., & Zhang, H. (2026) · Biochemical Pharmacology · doi:10.1016/j.bcp.2026.118545
Drosophila dendrites are resilient to adult-onset deficits in mitochondrial dynamics
Wang, H., Fortson, D. G., Donovan, E. J., Whitbeck, H. S., Robles, B., Wass, K., Bortey, L., Adler, A. J., Kalai, J. I., Napoleone, G., et al. (2026) · The Journal of Cell Biology · doi:10.1083/jcb.202511010
“…via piecemeal degradation of mitochondrial proteins and mitochondria-derived vesicles or via local mitophagy or macroautophagy followed by retrograde trafficking of autophagosomes (Ashrafi et al., 2014; Cason et al., 2022; Goldsmith et al., 2022; Maday et al., 2012; Misgeld and Schwarz, 2017).”
Metadata
- Authors
- Ashrafi, G., Schlehe, J. S., LaVoie, M. J., & Schwarz, T. L.
- Affiliations
- Boston Children's Hospital (US)
- Brigham and Women's Hospital (US)
- Corresponding author
- Schwarz, Thomas L.
- Venue
- Journal of Cell Biology
- Publisher
- Rockefeller University Press
- Published
- 2014-08-25
- Volume
- 206
- Issue
- 5
- Pages
- 655-670
- ISSN
- 0021-9525 (ISSN-L)
- 1540-8140
- PMC
- PMC4151150
- OpenAlex
- W1992264711
- Cited by
- 502
- References
- 65
- Citations by year
- 2026: 18 · 2025: 22 · 2024: 39 · 2023: 25 · 2022: 39 · 2021: 53 · 2020: 53 · 2019: 51 · 2018: 49 · 2017: 49 · 2016: 51 · 2015: 46 · 2014: 7
- FWCI
- 38.33
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- cc-by-nc-sa
- Locations
- The Journal of Cell Biology (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion, cc-by-nc-sa)
- PubMed (publishedVersion)
- Digital Access to Scholarship at Harvard (DASH) (Harvard University) (submittedVersion, cc-by)
- Funders
- National Institute of General Medical Sciences (GM069808, R01GM069808)
- National Institute of Neurological Disorders and Stroke (R21NS069949, R01NS065013, NS065013, NS069949)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (HD-01866, P30HD018655)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
- Health Sciences › Medicine › Clinical Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ubiquitin and proteasome pathways
- Keywords
- mitophagy, PINK1, Parkin, axons, mitochondrial damage, Parkinson's disease, autophagosomes, lysosomes, oxidative stress, neuroprotection, hippocampal neurons, retrograde transport, mitochondrial quality control
- MeSH terms
- PTEN-Induced Putative Kinase, Animals, Antimycin A, Autophagy, Axons, Cells, Cultured, Female, Lysosomes, Mice, Inbred C57BL, Microtubule-Associated Proteins, Mitochondria, Phagosomes, Protein Kinases, Veratridine, Rats, Sprague-Dawley, Mice, Knockout, Rats, Long-Evans, Protein Transport, Ubiquitin-Protein Ligases, Mice, Rats, Membrane Potential, Mitochondrial, Mice, 129 Strain, Mitophagy
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