Evidence map›Paper›PMID 28009276›Full record

ArticleNeuron2016

Mitochondria Localize to Injured Axons to Support Regeneration.

Sung Min Han, Huma S Baig, Marc Hammarlund

Abstract read
In one paragraph

Article in Neuron, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 150 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
150citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

150 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  7. Review
  8. Exercise-Induced Differential Transcriptional Output of AMPK Signaling Improves Axon Regeneration and Functional Recovery.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026
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  18. Stroke and vascular neurology · 2025
    Article
  19. Article
  20. In situ cavitation bubble manometry reveals a lack of light-activated guard cell turgor modulation in bryophytes.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article

90 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

3 authors.

Sung Min HanDepartments of Genetics and Neuroscience, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06510, USA.
Huma S BaigDepartments of Genetics and Neuroscience, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06510, USA.
Marc HammarlundDepartments of Genetics and Neuroscience, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06510, USA. Electronic address: marc.hammarlund@yale.edu.

Funding

Yale Clinical and Translational Science Award (U Component)UL1TR001863 · NCATS · YALE UNIVERSITY · PI John H. Krystal, LUCILA OHNO-MACHADO · 2016 to 2026
$102.9M
New Mechanisms in Axon RegenerationR01NS094219 · NINDS · YALE UNIVERSITY · PI HAMMARLUND, MARC · 2015 to 2025
$4.0M
Evaluation of Novel Axon Regeneration Targets for Spinal Cord injury TherapyR01NS098817 · NINDS · YALE UNIVERSITY · PI HAMMARLUND, MARC, STRITTMATTER, STEPHEN M · 2016 to 2020
$1.4M
Mechanisms and Regulation of Neuronal AgingR56AG050969 · NIA · YALE UNIVERSITY · PI HAMMARLUND, MARC, MILLER, DAVID M · 2016 to 2016
$606k
NCATS NIH HHS UL1 TR001863NIA NIH HHS R56 AG050969NINDS NIH HHS R01 NS094219NINDS NIH HHS R01 NS098817
6 · The paper itself

Abstract

Axon regeneration is essential to restore the nervous system after axon injury. However, the neuronal cell biology that underlies axon regeneration is incompletely understood. Here we use in vivo, single-neuron analysis to investigate the relationship between nerve injury, mitochondrial localization, and axon regeneration. Mitochondria translocate into injured axons so that average mitochondria density increases after injury. Moreover, single-neuron analysis reveals that axons that fail to increase mitochondria have poor regeneration. Experimental alterations to axonal mitochondrial distribution or mitochondrial respiratory chain function result in corresponding changes to regeneration outcomes. Axonal mitochondria are specifically required for growth-cone migration, identifying a key energy challenge for injured neurons. Finally, mitochondrial localization to the axon after injury is regulated in part by dual-leucine zipper kinase 1 (DLK-1), a conserved regulator of axon regeneration. These data identify regulation of axonal mitochondria as a new cell-biological mechanism that helps determine the regenerative response of injured neurons.

Indexed as

Nerve RegenerationAdenosine TriphosphateAnimalsAxonsBiological TransportCaenorhabditis elegansCaenorhabditis elegans ProteinsMAP Kinase Kinase KinasesMicroscopy, ConfocalMitochondriaMitogen-Activated Protein KinasesRegenerationAdenosine TriphosphateCaenorhabditis elegans ProteinsDLK-1 protein, C elegansMAP Kinase Kinase KinasesMitogen-Activated Protein Kinasesaxon regenerationC. elegansDLK-1MIROmitochondria

Identifiers

PMID28009276
PMCPMC5364819

What OpenQuestion holds

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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.