Evidence map›Paper›PMID 37224250›Full record

ArticleScience advances2023

Mitophagy restricts BAX/BAK-independent, Parkin-mediated apoptosis.

Giovanni Quarato, Luigi Mari, Nicholas J Barrows, Mao Yang, Sebastian Ruehl, Mark J Chen, Cliff S Guy, Jonathan Low, Taosheng Chen, Douglas R Green

Open access · goldAbstract read
In one paragraph

Article in Science advances, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
10.7field-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

38 citing papers in PubMed, 50 citations in OpenAlex.

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  14. Dual regulation of autophagy: paradoxical effects on tumor angiogenesis.Frontiers in cell and developmental biology · 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

10 authors at 1 institution in 1 country.

Giovanni QuaratoDepartment of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.ORCID 0000-0003-1167-3422
Luigi MariDepartment of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.ORCID 0000-0002-2903-7689
Nicholas J BarrowsDepartment of Chemical Biology and Therapeutics, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.
Mao YangDepartment of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.
Sebastian RuehlDepartment of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.
Mark J ChenDepartment of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.
Cliff S GuyDepartment of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.ORCID 0000-0001-7486-7107
Jonathan LowDepartment of Chemical Biology and Therapeutics, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.
Taosheng ChenDepartment of Chemical Biology and Therapeutics, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.ORCID 0000-0001-6420-3809
Douglas R GreenDepartment of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA.ORCID 0000-0002-7332-1417
St. Jude Children's Research Hospital · US

Funding

Viral Vector Technology (VVTSR)P30CA021765 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI Shondra Michelle Miller · 1985 to 2026
$166.9M
MECHANISMS OF REGULATED CELL DEATHR35CA231620 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI Douglas R. Green · 2018 to 2026
$9.2M
NCI NIH HHS P30 CA021765NCI NIH HHS R35 CA231620
6 · The paper itself

Abstract

Degradation of defective mitochondria is an essential process to maintain cellular homeostasis and it is strictly regulated by the ubiquitin-proteasome system (UPS) and lysosomal activities. Here, using genome-wide CRISPR and small interference RNA screens, we identified a critical contribution of the lysosomal system in controlling aberrant induction of apoptosis following mitochondrial damage. After treatment with mitochondrial toxins, activation of the PINK1-Parkin axis triggered a BAX- and BAK-independent process of cytochrome c release from mitochondria followed by APAF1 and caspase 9-dependent apoptosis. This phenomenon was mediated by UPS-dependent outer mitochondrial membrane (OMM) degradation and was reversed using proteasome inhibitors. We found that the subsequent recruitment of the autophagy machinery to the OMM protected cells from apoptosis, mediating the lysosomal degradation of dysfunctional mitochondria. Our results underscore a major role of the autophagy machinery in counteracting aberrant noncanonical apoptosis and identified autophagy receptors as key elements in the regulation of this process.

Indexed as

ApoptosisMitophagyAutophagybcl-2-Associated X ProteinMitochondriaUbiquitinbcl-2-Associated X ProteinUbiquitin

Identifiers

PMID37224250
PMCPMC10208567
OpenAlexW4378071265

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.