Evidence map›Paper›PMID 36691806›Full record

ArticleAutophagy2023

Endosomal-dependent mitophagy coordinates mitochondrial nucleoid and mtDNA elimination.

Ayesha Sen, Julia Boix, David Pla-Martín

Open access · greenAbstract readComment
In one paragraph

Article in Autophagy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

12 citing papers in PubMed, 15 citations in OpenAlex.

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  10. Mitochondrial DNA Damage and Its Repair Mechanisms in Aging Oocytes.International journal of molecular sciences · 2024
    Review
  11. Review
  12. Prohibitions in the meta-inflammatory response: a review.Frontiers in molecular biosciences · 2024
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Ayesha SenCenter for Physiology and Pathophysiology, Faculty of Medicine and University Hospital Cologne, University of Cologne, Cologne, Germany.
Julia BoixCenter for Physiology and Pathophysiology, Faculty of Medicine and University Hospital Cologne, University of Cologne, Cologne, Germany.
David Pla-MartínCenter for Physiology and Pathophysiology, Faculty of Medicine and University Hospital Cologne, University of Cologne, Cologne, Germany.ORCID 0000-0002-5189-0723
University of Cologne · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitophagy and its variants are considered important salvage pathways to remove dysfunctional mitochondria. Non-canonical mitophagy, independent of autophagosome formation and including endosomal-dependent mitophagy, operate upon specific injury. In a recent paper, we describe a new mechanism where, upon mtDNA damage, mitochondrial nucleoids are eliminated via an endosomal-mitophagy pathway. Using proximity proteomics, we identified the proteins required for elimination of mutated mitochondrial nucleoids from the mitochondrial matrix. Among them, ATAD3 and SAMM50 control cristae architecture and nucleoid interaction, necessary for mtDNA extraction. In the mitochondrial outer membrane, SAMM50 coordinates with the retromer protein VPS35 to sequester mtDNA in endosomes and guide them toward elimination, thus avoiding the activation of an exacerbated immune response. Here, we summarize our findings and examine how this newly described pathway contributes to our understanding of mtDNA quality control.

Indexed as

DNA, MitochondrialMitophagyAutophagyEndosomesMitochondriaMitochondrial ProteinsDNA, MitochondrialMitochondrial ProteinsendosomesMitophagymtDNA

Identifiers

PMID36691806
PMCPMC10392727
OpenAlexW4317871235

What OpenQuestion holds

Textmetadata
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.