Evidence map›Paper›PMID 39177530›Full record

ArticleAutophagy2025

Artificial targeting of autophagy components to mitochondria reveals both conventional and unconventional mitophagy pathways.

Katharina C Lorentzen, Alan R Prescott, Ian G Ganley

Abstract read
In one paragraph

Article in Autophagy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
–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

14 citing papers in PubMed.

  1. Article
  2. Emerging mechanisms of ATG8-independent non-canonical autophagy.Journal of physiology and biochemistry · 2026
    Review
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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.

Katharina C LorentzenMRC Protein Phosphorylation and Ubiquitylation Unit, University of Dundee, Dundee, UK.
Alan R PrescottDundee Imaging Facility, School of Life Sciences, University of Dundee, Dundee, UK.
Ian G GanleyMRC Protein Phosphorylation and Ubiquitylation Unit, University of Dundee, Dundee, UK.ORCID 0000-0003-1481-9407

Funding

Medical Research Council MC_UU_00018/2
6 · The paper itself

Abstract

Macroautophagy/autophagy enables lysosomal degradation of a diverse array of intracellular material. This process is essential for normal cellular function and its dysregulation is implicated in many diseases. Given this, there is much interest in understanding autophagic mechanisms of action in order to determine how it can be best targeted therapeutically. In mitophagy, the selective degradation of mitochondria via autophagy, mitochondria first need to be primed with signals that allow the recruitment of the core autophagy machinery to drive the local formation of an autophagosome around the target mitochondrion. To determine how the recruitment of different core autophagy components can drive mitophagy, we took advantage of the

Indexed as

AutophagyMitochondriaMitophagyAnimalsAutophagosomesAutophagy-Related Protein-1 HomologAutophagy-Related ProteinsHeLa CellsHumansLysosomesAutophagy-Related Protein-1 HomologAutophagy-Related ProteinsATG16L1Atg8nanobodytargeted organelle degradationULK1

Identifiers

PMID39177530
PMCPMC11760219

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.