ArticlePLoS computational biology2021
Optimizing mitochondrial maintenance in extended neuronal projections.
Article in PLoS computational biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Mitochondrial dynamics resolve physical-social tensions and challenges through adaptable multi-objective optimisation.bioRxiv : the preprint server for biology · 2026Article
- Start early and pack light: Collaborative adventures in theory and experiment.Seminars in cell & developmental biology · 2025Review
- Mitochondrial transport in symmetric and asymmetric axons with multiple branching junctions: a computational study.Computer methods in biomechanics and biomedical engineering · 2024Article
- Article
- Effect of mitochondrial circulation on mitochondrial age density distribution.International journal for numerical methods in biomedical engineering · 2023Article
- Aging, oxidative stress and degenerative diseases: mechanisms, complications and emerging therapeutic strategies.Biogerontology · 2023Review
- Effects of axon branching and asymmetry between the branches on transport, mean age, and age density distributions of mitochondria in neurons: A computational study.International journal for numerical methods in biomedical engineering · 2022Article
- Spatiotemporal analysis of axonal autophagosome-lysosome dynamics reveals limited fusion events and slow maturation.Molecular biology of the cell · 2022Article
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neurons rely on localized mitochondria to fulfill spatially heterogeneous metabolic demands. Mitochondrial aging occurs on timescales shorter than the neuronal lifespan, necessitating transport of fresh material from the soma. Maintaining an optimal distribution of healthy mitochondria requires an interplay between a stationary pool localized to sites of high metabolic demand and a motile pool capable of delivering new material. Interchange between these pools can occur via transient fusion / fission events or by halting and restarting entire mitochondria. Our quantitative model of neuronal mitostasis identifies key parameters that govern steady-state mitochondrial health at discrete locations. Very infrequent exchange between stationary and motile pools optimizes this system. Exchange via transient fusion allows for robust maintenance, which can be further improved by selective recycling through mitophagy. These results provide a framework for quantifying how perturbations in organelle transport and interactions affect mitochondrial homeostasis in neurons, a key aspect underlying many neurodegenerative disorders.
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Registered trials
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