Evidence map›Paper›PMID 35051374›Full record

ArticleNeuron2022

Brain-derived autophagosome profiling reveals the engulfment of nucleoid-enriched mitochondrial fragments by basal autophagy in neurons.

Juliet Goldsmith, Alban Ordureau, J Wade Harper, Erika L F Holzbaur

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in Neuron, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
15.7field-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

64 citing papers in PubMed, 104 citations in OpenAlex.

  1. Article
  2. The role of impaired mitochondrial function in neurological manifestations of mitochondrial diseases.Mammalian genome : official journal of the International Mammalian Genome Society · 2026
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  12. Self-renewal of neuronal mitochondria through asymmetric division.bioRxiv : the preprint server for biology · 2025
    Article
  13. bioRxiv : the preprint server for biology · 2025
    Article
  14. Article
  15. Article
  16. Autophagic stress activates distinct compensatory secretory pathways in neurons.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  17. Review
  18. Article
  19. Review
  20. Article

4 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Juliet GoldsmithDepartment of Physiology, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104, USA.
Alban OrdureauDepartment of Cell Biology, Blavatnik Institute, Harvard Medical School, Boston, MA 02115, USA.
J Wade HarperDepartment of Cell Biology, Blavatnik Institute, Harvard Medical School, Boston, MA 02115, USA.
Erika L F HolzbaurDepartment of Physiology, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104, USA. Electronic address: holzbaur@pennmedicine.upenn.edu.
Harvard University · USUniversity of Pennsylvania · US

Funding

Endolysosomal Proteome Landscapes Through the Lens of Neurodegenerative Risk AllelesR01NS110395 · NINDS · HARVARD MEDICAL SCHOOL · PI JEFFREY W HARPER · 2018 to 2026
$4.1M
Mechanistic analysis of axonal transport defects in motor neuron degenerative disR01NS060698 · NINDS · UNIVERSITY OF PENNSYLVANIA · PI HOLZBAUR, ERIKA L · 2008 to 2025
$3.8M
Systematic discovery and functional analysis of the PARKIN modified proteomeR37NS083524 · NINDS · HARVARD MEDICAL SCHOOL · PI HARPER, JEFFREY W · 2013 to 2019
$3.0M
Mechanistic analysis of axonal transport defects in neurodegenerative diseaseR37NS060698 · NINDS · UNIVERSITY OF PENNSYLVANIA · PI HOLZBAUR, ERIKA L · 2014 to 2020
$2.9M
Regulation of PINK1 and PARKIN-Dependent MitophagyR01NS083524 · NINDS · HARVARD MEDICAL SCHOOL · PI HARPER, JEFFREY W · 2020 to 2024
$2.2M
NINDS NIH HHS R01 NS060698NINDS NIH HHS R01 NS083524NINDS NIH HHS R01 NS110395NINDS NIH HHS R37 NS060698NINDS NIH HHS R37 NS083524
6 · The paper itself

Abstract

Neurons depend on autophagy to maintain cellular homeostasis, and defects in autophagy are pathological hallmarks of neurodegenerative disease. To probe the role of basal autophagy in the maintenance of neuronal health, we isolated autophagic vesicles from mouse brain tissue and used proteomics to identify the major cargos engulfed within autophagosomes, validating our findings in rodent primary and human iPSC-derived neurons. Mitochondrial proteins were identified as a major cargo in the absence of mitophagy adaptors such as OPTN. We found that nucleoid-associated proteins are enriched compared with other mitochondrial components. In the axon, autophagic engulfment of nucleoid-enriched mitochondrial fragments requires the mitochondrial fission machinery Drp1. We proposed that localized Drp1-dependent fission of nucleoid-enriched fragments in proximity to the sites of autophagosome biogenesis enhances their capture. The resulting efficient autophagic turnover of nucleoids may prevent accumulation of mitochondrial DNA in the neuron, thus mitigating activation of proinflammatory pathways that contribute to neurodegeneration.

Indexed as

AutophagosomesNeurodegenerative DiseasesAnimalsAutophagyBrainMiceNeuronsautophagyDrp1mitochondriamitochondrial divisionmitochondrial nucleoidsmitophagyneurodegenerationneuronal homeostasisTFAM

Identifiers

PMID35051374
PMCPMC8930448
OpenAlexW4205256619

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.