Evidence map›Paper›PMID 42869959›Full record

ArticleLeukemia2026

Inhibition of PHB2/PINK1-mediated mitophagy potentiates venetoclax activity in acute myeloid leukemia.

Romain Vazquez, Maxime Sajot, Jad Nasrallah, Rudy Birsen, Ismaël Boussaid, Morgane Plevenage, Zubaidan Tuerdi, Axelle Guedon, Lilia Cantero Aguilar, Tony Huynh and 14 more

Abstract read
PubMed Publisher
In one paragraph

Article in Leukemia, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

24 authors.

Romain VazquezUniversité Paris Cité, Institut Cochin, CNRSUMR8104, INSERM U1016, a member of OPALE Carnot Institute, The Organization for Partnerships in Leukemia, Paris, France.
Maxime SajotCancer Research Center of Toulouse, UMR1037-INSERM, Toulouse, France.
Jad NasrallahUniversité Paris Cité, Institut Cochin, CNRSUMR8104, INSERM U1016, a member of OPALE Carnot Institute, The Organization for Partnerships in Leukemia, Paris, France.
Rudy BirsenUniversité Paris Cité, Institut Cochin, CNRSUMR8104, INSERM U1016, a member of OPALE Carnot Institute, The Organization for Partnerships in Leukemia, Paris, France.
Ismaël BoussaidUniversité Paris Cité, Institut Cochin, CNRSUMR8104, INSERM U1016, a member of OPALE Carnot Institute, The Organization for Partnerships in Leukemia, Paris, France.ORCID http://orcid.org/0000-0002-1839-8411
Morgane PlevenageUniversité Paris Cité, Institut Cochin, CNRSUMR8104, INSERM U1016, a member of OPALE Carnot Institute, The Organization for Partnerships in Leukemia, Paris, France.ORCID http://orcid.org/0009-0003-8150-9959
Zubaidan TuerdiUniversité Paris Cité, Institut Cochin, CNRSUMR8104, INSERM U1016, a member of OPALE Carnot Institute, The Organization for Partnerships in Leukemia, Paris, France.
Axelle GuedonUniversité Paris Cité, Institut Cochin, CNRSUMR8104, INSERM U1016, a member of OPALE Carnot Institute, The Organization for Partnerships in Leukemia, Paris, France.
Lilia Cantero AguilarUniversité Paris Cité, Institut Cochin, CNRSUMR8104, INSERM U1016, a member of OPALE Carnot Institute, The Organization for Partnerships in Leukemia, Paris, France.
Tony HuynhUniversité Paris Cité, Institut Cochin, CNRSUMR8104, INSERM U1016, a member of OPALE Carnot Institute, The Organization for Partnerships in Leukemia, Paris, France.
Natacha JohnsonUniversité Paris Cité, Institut Cochin, CNRSUMR8104, INSERM U1016, a member of OPALE Carnot Institute, The Organization for Partnerships in Leukemia, Paris, France.
Chloé FriedrichUniversité Paris Cité, Institut Cochin, CNRSUMR8104, INSERM U1016, a member of OPALE Carnot Institute, The Organization for Partnerships in Leukemia, Paris, France.
Eric GrignanoUniversité Paris Cité, Institut Cochin, CNRSUMR8104, INSERM U1016, a member of OPALE Carnot Institute, The Organization for Partnerships in Leukemia, Paris, France.
Justine DecroocqUniversité Paris Cité, Institut Cochin, CNRSUMR8104, INSERM U1016, a member of OPALE Carnot Institute, The Organization for Partnerships in Leukemia, Paris, France.
Lise WillemsUniversité Paris Cité, Institut Cochin, CNRSUMR8104, INSERM U1016, a member of OPALE Carnot Institute, The Organization for Partnerships in Leukemia, Paris, France.ORCID http://orcid.org/0000-0001-7866-2571
Carole AlmireUniversité Paris Cité, Institut Cochin, CNRSUMR8104, INSERM U1016, a member of OPALE Carnot Institute, The Organization for Partnerships in Leukemia, Paris, France.
Marie-Clotilde Alves-GuerraUniversité Paris Cité, Institut Cochin, CNRSUMR8104, INSERM U1016, a member of OPALE Carnot Institute, The Organization for Partnerships in Leukemia, Paris, France.ORCID http://orcid.org/0000-0002-7918-1216
Evelyne LauretUniversité Paris Cité, Institut Cochin, CNRSUMR8104, INSERM U1016, a member of OPALE Carnot Institute, The Organization for Partnerships in Leukemia, Paris, France.
Yannick SimoniUniversité Paris Cité, Institut Cochin, CNRSUMR8104, INSERM U1016, a member of OPALE Carnot Institute, The Organization for Partnerships in Leukemia, Paris, France.
Michaela FontenayUniversité Paris Cité, Institut Cochin, CNRSUMR8104, INSERM U1016, a member of OPALE Carnot Institute, The Organization for Partnerships in Leukemia, Paris, France.ORCID http://orcid.org/0000-0002-5492-6349
Olivier KosmiderUniversité Paris Cité, Institut Cochin, CNRSUMR8104, INSERM U1016, a member of OPALE Carnot Institute, The Organization for Partnerships in Leukemia, Paris, France.ORCID http://orcid.org/0000-0002-6021-4057
Didier BouscaryUniversité Paris Cité, Institut Cochin, CNRSUMR8104, INSERM U1016, a member of OPALE Carnot Institute, The Organization for Partnerships in Leukemia, Paris, France.
Clement LarrueCancer Research Center of Toulouse, UMR1037-INSERM, Toulouse, France.
Nicolas ChapuisUniversité Paris Cité, Institut Cochin, CNRSUMR8104, INSERM U1016, a member of OPALE Carnot Institute, The Organization for Partnerships in Leukemia, Paris, France. nicolas.chapuis@aphp.fr.ORCID http://orcid.org/0000-0003-0601-3948

Funding

Fondation pour la Recherche Médicale (Foundation for Medical Research in France) FDM202106013429
6 · The paper itself

Abstract

Acute myeloid leukemia (AML) cells are highly dependent on mitochondrial activity for survival, with this metabolic reliance driven in part by BCL-2, which is therapeutically targeted by venetoclax-based therapies. The regulation of mitochondrial dynamics in leukemic cells is therefore essential for maintaining mitochondrial homeostasis. However, the mechanisms that enable selective degradation of damaged mitochondria (mitophagy) are still poorly understood in AML. In this study, we sought to elucidate the role of PTEN-induced putative kinase 1 (PINK1), a key sensor of mitochondrial stress, in regulating mitophagy in leukemic cells. Our results identified PINK1 as a central modulator of mitophagy. Genetic depletion of PINK1 reduced both basal and stress-induced mitophagy, leading to mitochondria accumulation and functional impairment. Additionally, we discovered that PINK1 stabilization during mitochondrial stress is regulated by Prohibitin 2 (PHB2), and that depletion or inhibition of PHB2 mirrored the biological effects of PINK1 loss. Notably, both genetic depletion of PINK1 or PHB2, as well as pharmacological inhibition of PHB2, significantly increased AML cell sensitivity to venetoclax both in vitro and in vivo. Together, these findings highlight the potential of targeting the PHB2/PINK1 signalling pathway to improve the efficacy of venetoclax-based therapies in AML by disrupting the mitophagy process.

Identifiers

PMID42869959

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.