Evidence map›Paper›PMID 25612908›Full record

ReviewExperimental cell research2015

Regulation of mitochondrial transport in neurons.

Mei-Yao Lin, Zu-Hang Sheng

Open access · greenAbstract readReview
In one paragraph

Review in Experimental cell research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 118 papers.

0numbers the graph read from it
0cells of the map it votes in
118citing papers in PubMed
10.4field-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

118 citing papers in PubMed, 218 citations in OpenAlex.

  1. Article
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  5. ATL2 Recruits TRAK1 to Promote Mitochondrial Transport at ER-Mitochondria Contact Sites.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  6. Mitochondrial mechanics nucleates axonal jamming and swelling.bioRxiv : the preprint server for biology · 2026
    Article
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  8. Review
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  13. Review
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58 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.

Mei-Yao LinSynaptic Function Section, The Porter Neuroscience Research Center, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Room 2B-215, 35 Convent Drive, Bethesda, MD 20892-3706, USA.
Zu-Hang ShengSynaptic Function Section, The Porter Neuroscience Research Center, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Room 2B-215, 35 Convent Drive, Bethesda, MD 20892-3706, USA. Electronic address: shengz@ninds.nih.gov.
National Institute of Neurological Disorders and Stroke · USNational 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
Intramural NIH HHS ZIA NS003029NINDS NIH HHS NS003029-08 DIR
6 · The paper itself

Abstract

Mitochondria are cellular power plants that supply ATP to power various biological activities essential for neuronal growth, survival, and function. Due to unique morphological features, neurons face exceptional challenges to maintain ATP and Ca(2+) homeostasis. Neurons require specialized mechanisms distributing mitochondria to distal areas where energy and Ca(2+) buffering are in high demand, such as synapses and axonal branches. These distal compartments also undergo development- and activity-dependent remodeling, thereby altering mitochondrial trafficking and distribution. Mitochondria move bi-directionally, pause briefly, and move again, frequently changing direction. In mature neurons, only one-third of axonal mitochondria are motile. Stationary mitochondria serve as local energy sources and buffer intracellular Ca(2+). The balance between motile and stationary mitochondria responds quickly to changes in axonal and synaptic physiology. Furthermore, neurons are postmitotic cells surviving for the lifetime of the organism; thus, mitochondria need to be removed when they become aged or dysfunction. Mitochondria also alter their motility under stress conditions or when their integrity is impaired. Therefore, regulation of mitochondrial transport is essential to meet altered metabolic requirements and to remove aged and damaged mitochondria or replenish healthy ones to distal terminals. Defects in mitochondrial transport and altered distribution are implicated in the pathogenesis of several major neurological disorders. Thus, research into the mechanisms regulating mitochondrial motility is an important emerging frontier in neurobiology. This short review provides an updated overview on motor-adaptor machineries that drive and regulate mitochondrial transport and docking receptors that anchor axonal mitochondria in response to the changes in synaptic activity, metabolic requirement, and altered mitochondrial integrity. The review focuses on microtubule (MT)-based mitochondrial trafficking and anchoring. Additional insight from different perspectives can be found in other in-depth reviews.

Indexed as

AnimalsBiological TransportHumansMitochondriaMolecular Motor ProteinsNeuronsSignal TransductionMolecular Motor ProteinsDynein motorsKinesin motorsMitochondrial dockingMitochondrial transportMitophagyMotile mitochondriaStationary mitochondriaSynaptic activitySyntaphilin

Identifiers

PMID25612908
PMCPMC4433773
OpenAlexW1984510450

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.