Evidence map›Paper›PMID 22619228›Full record

ReviewJournal of cell science2012

The axonal transport of mitochondria.

William M Saxton, Peter J Hollenbeck

Abstract readReview
In one paragraph

Review in Journal of cell science, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 293 papers.

0numbers the graph read from it
0cells of the map it votes in
293citing papers in PubMed
43.8field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

293 citing papers in PubMed, 1,194 citations in OpenAlex.

  1. Review
  2. The role of impaired mitochondrial function in neurological manifestations of mitochondrial diseases.Mammalian genome : official journal of the International Mammalian Genome Society · 2026
    Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
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  10. Mitochondrial mechanics nucleates axonal jamming and swelling.bioRxiv : the preprint server for biology · 2026
    Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Pathway-Specific Ultrastructure of Thalamocortical Synapses in Mouse Somatosensory Area S2.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Article

233 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 1 country.

William M SaxtonDepartment of Molecular Cell and Developmental Biology, University of California, Cruz, CA 95060, USA. bsaxton@ucsc.edu
Peter J Hollenbeck
State Street (United States) · USUniversity of California, Santa Cruz · US

Funding

MECHANISMS AND FUNCTIONS OF SUBCELLULAR MOTILITYR01GM046295 · NIGMS · UNIVERSITY OF CALIFORNIA SANTA CRUZ · PI SAXTON, WILLIAM M · 1991 to 2016
$3.7M
CONTROL OF NEURONAL ORGANELLE TRANSPORTR01NS027073 · NINDS · PURDUE UNIVERSITY WEST LAFAYETTE · PI HOLLENBECK, PETER J. · 1990 to 2013
$3.6M
NIGMS NIH HHS R01 GM046295NINDS NIH HHS R01 NS027073
6 · The paper itself

Abstract

Vigorous transport of cytoplasmic components along axons over substantial distances is crucial for the maintenance of neuron structure and function. The transport of mitochondria, which serves to distribute mitochondrial functions in a dynamic and non-uniform fashion, has attracted special interest in recent years following the discovery of functional connections among microtubules, motor proteins and mitochondria, and their influences on neurodegenerative diseases. Although the motor proteins that drive mitochondrial movement are now well characterized, the mechanisms by which anterograde and retrograde movement are coordinated with one another and with stationary axonal mitochondria are not yet understood. In this Commentary, we review why mitochondria move and how they move, focusing particularly on recent studies of transport regulation, which implicate control of motor activity by specific cell-signaling pathways, regulation of motor access to transport tracks and static microtubule-mitochondrion linkers. A detailed mechanism for modulating anterograde mitochondrial transport has been identified that involves Miro, a mitochondrial Ca(2+)-binding GTPase, which with associated proteins, can bind and control kinesin-1. Elements of the Miro complex also have important roles in mitochondrial fission-fusion dynamics, highlighting questions about the interdependence of biogenesis, transport, dynamics, maintenance and degradation.

Indexed as

AnimalsAxonal TransportAxonsCalciumDrosophila melanogasterHumansMembrane FusionMicrotubulesMitochondriaMitochondrial ProteinsMolecular Motor ProteinsNeurodegenerative DiseasesProtein Bindingrho GTP-Binding ProteinsSignal TransductionCalciumMitochondrial ProteinsMolecular Motor Proteinsrho GTP-Binding ProteinsRHOT1 protein, human

Identifiers

PMID22619228
PMCPMC3656622
OpenAlexW2055572268

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.