Evidence map›Paper›PMID 27268498›Full record

ArticleThe Journal of cell biology2016

Facilitation of axon regeneration by enhancing mitochondrial transport and rescuing energy deficits.

Bing Zhou, Panpan Yu, Mei-Yao Lin, Tao Sun, Yanmin Chen, Zu-Hang Sheng

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 198 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
198citing papers in PubMed, 1 pooled it
15.9field-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

198 citing papers in PubMed, 1 synthesis or guideline pooled it, 314 citations in OpenAlex.

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138 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

6 authors at 2 institutions in 2 countries.

Bing ZhouSynaptic Functions Section, The Porter Neuroscience Research Center, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.ORCID 0000-0002-7718-2311
Panpan YuGuangdong-Hong Kong-Macau Institute of CNS Regeneration, Ministry of Education Joint International Research Laboratory of CNS Regeneration, Jinan University, Guangzhou 510632, China.
Mei-Yao LinSynaptic Functions Section, The Porter Neuroscience Research Center, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.
Tao SunSynaptic Functions Section, The Porter Neuroscience Research Center, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.ORCID 0000-0002-7834-0721
Yanmin ChenSynaptic Functions Section, The Porter Neuroscience Research Center, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.
Zu-Hang ShengSynaptic Functions Section, The Porter Neuroscience Research Center, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892 shengz@ninds.nih.gov.
National Institutes of Health · USJinan University · CN

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
Intramural NIH HHS ZIA NS002946Intramural NIH HHS ZIA NS003029
6 · The paper itself

Abstract

Although neuronal regeneration is a highly energy-demanding process, axonal mitochondrial transport progressively declines with maturation. Mature neurons typically fail to regenerate after injury, thus raising a fundamental question as to whether mitochondrial transport is necessary to meet enhanced metabolic requirements during regeneration. Here, we reveal that reduced mitochondrial motility and energy deficits in injured axons are intrinsic mechanisms controlling regrowth in mature neurons. Axotomy induces acute mitochondrial depolarization and ATP depletion in injured axons. Thus, mature neuron-associated increases in mitochondria-anchoring protein syntaphilin (SNPH) and decreases in mitochondrial transport cause local energy deficits. Strikingly, enhancing mitochondrial transport via genetic manipulation facilitates regenerative capacity by replenishing healthy mitochondria in injured axons, thereby rescuing energy deficits. An in vivo sciatic nerve crush study further shows that enhanced mitochondrial transport in snph knockout mice accelerates axon regeneration. Understanding deficits in mitochondrial trafficking and energy supply in injured axons of mature neurons benefits development of new strategies to stimulate axon regeneration.

Indexed as

Axonal TransportEnergy MetabolismNerve RegenerationAdenosine DiphosphateAdenosine TriphosphateAnimalsAxonsAxotomyCell DifferentiationGAP-43 ProteinGrowth ConesMembrane Potential, MitochondrialMembrane ProteinsMice, Inbred C57BLMice, KnockoutMicrotubule-Associated ProteinsAdenosine DiphosphateAdenosine TriphosphateGAP-43 ProteinMembrane ProteinsMicrotubule-Associated ProteinsNerve Tissue ProteinsSnph protein, mouse

Identifiers

PMID27268498
PMCPMC4932375
OpenAlexW2410831727

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.