Evidence map›Paper›PMID 19341731›Full record

ReviewExperimental neurology2009

Mitochondrial transport and docking in axons.

Qian Cai, Zu-Hang Sheng

Abstract readReview
In one paragraph

Review in Experimental neurology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 1 pooled it
4.2field-weighted citation impact, top 5% 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

49 citing papers in PubMed, 1 synthesis or guideline pooled it, 98 citations in OpenAlex.

  1. Pooled it
  2. Review
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    Article
  4. Review
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  6. Underneath the Gut-Brain Axis in IBD-Evidence of the Non-Obvious.International journal of molecular sciences · 2024
    Review
  7. Review
  8. Review
  9. Nano-positioning and tubulin conformation contribute to axonal transport regulation of mitochondria along microtubules.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Review
  16. Axonal Transport and Mitochondrial Function in Neurons.Frontiers in cellular neuroscience · 2019
    Review
  17. Article
  18. Optic Nerve Head Drusen: An Update.Neuro-ophthalmology (Aeolus Press) · 2018
    Review
  19. Article
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Qian CaiSynaptic Function Section, The Porter Neuroscience Research Center, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, USA. caiq@ninds.nih.gov
Zu-Hang Sheng
National Institutes of Health · US

Funding

Regulation of mitochondrial transport and its impact on synaptic transmissionZIANS003029 · NINDS · NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE · PI SHENG, ZU-HANG · 2009 to 2025
$31.5M
Transport and regulation of presynaptic release machineryZIANS002946 · NINDS · NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE · PI SHENG, ZU-HANG · 2009 to 2025
$25.6M
Axonal mitochondrial mobility and its impact on synaptic transmissionZ01NS003029 · NINDS · NEUROLOGICAL DISORDERS AND STROKE · PI SHENG, ZU-HANG · 2007 to 2008
$2.1M
Intramural NIH HHS Z01 NS003029
6 · The paper itself

Abstract

Proper transport and distribution of mitochondria in axons and at synapses are critical for the normal physiology of neurons. Mitochondria in axons display distinct motility patterns and undergo saltatory and bidirectional movement, where mitochondria frequently stop, start moving again, and change direction. While approximately one-third of axonal mitochondria are mobile in mature neurons, a large proportion remains stationary. Their net movement is significantly influenced by recruitment to stationary or motile states. In response to the diverse physiological states of axons and synapses, the mitochondrial balance between motile and stationary phases is a possible target of regulation by intracellular signals and synaptic activity. Efficient control of mitochondrial retention (docking) at particular stations, where energy production and calcium homeostasis capacity are highly demanded, is likely essential for neuronal development and function. In this review, we introduce the molecular and cellular mechanisms underlying the complex mobility patterns of axonal mitochondria and discuss how motor adaptor complexes and docking machinery contribute to mitochondrial transport and distribution in axons and at synapses. In addition, we briefly discuss the physiological evidence how axonal mitochondrial mobility impacts synaptic function.

Indexed as

AnimalsAxonal TransportAxonsHumansIntracellular Signaling Peptides and ProteinsMembrane ProteinsMicrotubule-Associated ProteinsMitochondriaMolecular Motor ProteinsNerve Tissue ProteinsNeuronsSignal TransductionVesicular Transport ProteinsIntracellular Signaling Peptides and ProteinsMembrane ProteinsMicrotubule-Associated ProteinsMolecular Motor ProteinsNerve Tissue ProteinsSNPH protein, humanSYBU protein, humanVesicular Transport Proteins

Identifiers

PMID19341731
PMCPMC2710402
OpenAlexW2051006825

What OpenQuestion holds

Textmetadata
LicenceTDM
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.