Evidence map›Paper›PMID 35642724›Full record

ArticleAging cell2022

MAPK15 protects from oxidative stress-dependent cellular senescence by inducing the mitophagic process.

Lorenzo Franci, Alessandro Tubita, Franca Maria Bertolino, Alessandro Palma, Giuseppe Cannino, Carmine Settembre, Andrea Rasola, Elisabetta Rovida, Mario Chiariello

Open access · goldAbstract read
In one paragraph

Article in Aging cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
5.8field-weighted citation impact, top 3% 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

20 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
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  6. Improving our understanding of the biology of aging: findings from the Age-It Research Program.The journals of gerontology. Series B, Psychological sciences and social sciences · 2025
    Article
  7. Article
  8. MAPK15 PreventsInternational journal of molecular sciences · 2025
    Article
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  12. Review
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  14. Article
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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

9 authors at 6 institutions in 1 country.

Lorenzo FranciIstituto di Fisiologia Clinica (IFC), Consiglio Nazionale delle Ricerche (CNR), Siena, Italy.ORCID 0000-0001-6300-1746
Alessandro TubitaDepartment of Experimental and Clinical Biomedical Sciences, University of Firenze, Firenze, Italy.
Franca Maria BertolinoIstituto di Fisiologia Clinica (IFC), Consiglio Nazionale delle Ricerche (CNR), Siena, Italy.
Alessandro PalmaDepartment of Onco-hematology, Gene and Cell Therapy, Bambino Gesù Children's Hospital-IRCCS, Rome, Italy.
Giuseppe CanninoDepartment of Biomedical Sciences, University of Padova, Padova, Italy.
Carmine SettembreTelethon Institute of Genetics and Medicine (TIGEM), Pozzuoli, Italy.
Andrea RasolaDepartment of Biomedical Sciences, University of Padova, Padova, Italy.
Elisabetta RovidaDepartment of Experimental and Clinical Biomedical Sciences, University of Firenze, Firenze, Italy.
Mario ChiarielloIstituto di Fisiologia Clinica (IFC), Consiglio Nazionale delle Ricerche (CNR), Siena, Italy.ORCID 0000-0001-8434-5177
Istituto per lo Studio e la Prevenzione Oncologica · ITUniversity of Florence · ITUniversity of Padua · ITBambino Gesù Children's Hospital · ITFederico II University Hospital · ITUniversity of Siena · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondria are the major source of reactive oxygen species (ROS), whose aberrant production by dysfunctional mitochondria leads to oxidative stress, thus contributing to aging as well as neurodegenerative disorders and cancer. Cells efficiently eliminate damaged mitochondria through a selective type of autophagy, named mitophagy. Here, we demonstrate the involvement of the atypical MAP kinase family member MAPK15 in cellular senescence, by preserving mitochondrial quality, thanks to its ability to control mitophagy and, therefore, prevent oxidative stress. We indeed demonstrate that reduced MAPK15 expression strongly decreases mitochondrial respiration and ATP production, while increasing mitochondrial ROS levels. We show that MAPK15 controls the mitophagic process by stimulating ULK1-dependent PRKN Ser

Indexed as

Cellular SenescenceExtracellular Signal-Regulated MAP KinasesMitophagyAutophagyHumansOxidative StressReactive Oxygen SpeciesExtracellular Signal-Regulated MAP KinasesMAPK15 protein, humanReactive Oxygen Speciesautophagycellular senescenceMAP kinasesmitophagyOxidative DNA damagesignal transduction

Identifiers

PMID35642724
PMCPMC9282834
OpenAlexW4281774075

What OpenQuestion 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 OpenQuestion graph.