Evidence map›Paper›PMID 29096078›Full record

ReviewNeuron2017

Mitostasis in Neurons: Maintaining Mitochondria in an Extended Cellular Architecture.

Thomas Misgeld, Thomas L Schwarz

Abstract readReview
In one paragraph

Review in Neuron, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 334 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
334citing papers in PubMed, 3 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

334 citing papers in PubMed, 3 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Article
  5. Article
  6. The role of impaired mitochondrial function in neurological manifestations of mitochondrial diseases.Mammalian genome : official journal of the International Mammalian Genome Society · 2026
    Review
  7. International journal of molecular sciences · 2026
    Review
  8. Review
  9. Mitochondrial molecular diversity in the brain.Current opinion in neurobiology · 2026
    Review
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article

274 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.

Thomas MisgeldTechnical University of Munich, Institute of Neuronal Cell Biology, Munich, Germany; German Center for Neurodegenerative Diseases, Munich, Germany; Munich Cluster for Systems Neurology, Munich, Germany; Center of Integrated Protein Science, Munich, Germany. Electronic address: thomas.misgeld@tum.de.
Thomas L SchwarzDepartment of Neurobiology, Harvard Medical School, Boston, MA, USA; F.M. Kirby Neurobiology Center, Children's Hospital, Boston, MA, USA. Electronic address: thomas.schwarz@childrens.harvard.edu.

Funding

Milton/Trak 1/2 Protein and the Transport of MitochondriaR01GM069808 · NIGMS · CHILDREN'S HOSPITAL BOSTON · PI SCHWARZ, THOMAS L. · 2004 to 2022
$5.2M
European Research Council 616791NIGMS NIH HHS R01 GM069808
6 · The paper itself

Abstract

Neurons have more extended and complex shapes than other cells and consequently face a greater challenge in distributing and maintaining mitochondria throughout their arbors. Neurons can last a lifetime, but proteins turn over rapidly. Mitochondria, therefore, need constant rejuvenation no matter how far they are from the soma. Axonal transport of mitochondria and mitochondrial fission and fusion contribute to this rejuvenation, but local protein synthesis is also likely. Maintenance of a healthy mitochondrial population also requires the clearance of damaged proteins and organelles. This involves degradation of individual proteins, sequestration in mitochondria-derived vesicles, organelle degradation by mitophagy and macroautophagy, and in some cases transfer to glial cells. Both long-range transport and local processing are thus at work in achieving neuronal mitostasis-the maintenance of an appropriately distributed pool of healthy mitochondria for the duration of a neuron's life. Accordingly, defects in the processes that support mitostasis are significant contributors to neurodegenerative disorders.

Indexed as

AnimalsHumansMitochondriaMitophagyNeurodegenerative DiseasesNeuronsaxonal transporthomeostasismitochondriamitophagyneurons

Identifiers

PMID29096078
PMCPMC5687842

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.