Evidence map›Paper›PMID 40272400›Full record

ArticleeLife2025

RAS-p110α signalling in macrophages is required for effective inflammatory response and resolution of inflammation.

Alejandro Rosell, Agata Adelajda Krygowska, Marta Alcón Pérez, Cristina Cuesta, Mathieu-Benoit Voisin, Juan de Paz, Héctor Sanz-Fraile, Vinothini Rajeeve, Ana Carreras-González, Alberto Berral-González and 9 more

Abstract read
In one paragraph

Article in eLife, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
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

19 authors.

Alejandro Rosell *Tumour-Stroma Signalling Lab., Centro de Investigación del Cáncer, Instituto de Biología Molecular y Celular del Cáncer, Consejo Superior de Investigaciones Científicas (CSIC)-Universidad de Salamanca, Campus Miguel de Unamuno, Salamanca, Spain.
Agata Adelajda Krygowska *Centre for Cancer and Inflammation, Barts Cancer Institute, Queen Mary University of London, London, United Kingdom.
Marta Alcón PérezTumour-Stroma Signalling Lab., Centro de Investigación del Cáncer, Instituto de Biología Molecular y Celular del Cáncer, Consejo Superior de Investigaciones Científicas (CSIC)-Universidad de Salamanca, Campus Miguel de Unamuno, Salamanca, Spain.
Cristina CuestaTumour-Stroma Signalling Lab., Centro de Investigación del Cáncer, Instituto de Biología Molecular y Celular del Cáncer, Consejo Superior de Investigaciones Científicas (CSIC)-Universidad de Salamanca, Campus Miguel de Unamuno, Salamanca, Spain.
Mathieu-Benoit VoisinCentre for Microvascular Research, William Harvey Research Institute, Queen Mary University of London, London, United Kingdom.ORCID https://orcid.org/0000-0003-3001-0894
Juan de PazTumour-Stroma Signalling Lab., Centro de Investigación del Cáncer, Instituto de Biología Molecular y Celular del Cáncer, Consejo Superior de Investigaciones Científicas (CSIC)-Universidad de Salamanca, Campus Miguel de Unamuno, Salamanca, Spain.
Héctor Sanz-FraileUnit of Biophysics and Bioengineering, Department of Biomedicine, School of Medicine and Health Sciences, Universitat de Barcelona, Barcelona, Spain.
Vinothini RajeeveCentre for Cancer Genomics and Computational Biology, Cell Signalling and Proteomics Laboratory, Barts Cancer Institute, Queen Mary University of London, London, United Kingdom.ORCID https://orcid.org/0000-0002-6361-4291
Ana Carreras-GonzálezBioinformatics and Functional Genomics, Centro de Investigación del Cáncer, Instituto de Biología Molecular y Celular del Cáncer, Consejo Superior de Investigaciones Científicas (CSIC)-Universidad de Salamanca, Salamanca, Spain.
Alberto Berral-GonzálezInflammation and Macrophage Plasticity Lab, CIC bioGUNE, Derio, Spain.
Ottilie SwinyardCentre for Cancer and Inflammation, Barts Cancer Institute, Queen Mary University of London, London, United Kingdom.
Enrique Gabandé-RodríguezCentre for Cancer and Inflammation, Barts Cancer Institute, Queen Mary University of London, London, United Kingdom.ORCID https://orcid.org/0000-0002-9715-8714
Julian DownwardOncogene Biology Laboratory, Francis Crick Institute, London, United Kingdom.
Jordi AlcarazUnit of Biophysics and Bioengineering, Department of Biomedicine, School of Medicine and Health Sciences, Universitat de Barcelona, Barcelona, Spain.
Juan AnguitaInflammation and Macrophage Plasticity Lab, CIC bioGUNE, Derio, Spain.
Carmen García-MacíasPathology Unit, Centro de Investigación del Cáncer, Instituto de Biología Molecular y Celular del Cáncer, Universidad de Salamanca, Salamanca, Spain.
Javier De Las RivasBioinformatics and Functional Genomics, Centro de Investigación del Cáncer, Instituto de Biología Molecular y Celular del Cáncer, Consejo Superior de Investigaciones Científicas (CSIC)-Universidad de Salamanca, Salamanca, Spain.
Pedro R CutillasCentre for Cancer Genomics and Computational Biology, Cell Signalling and Proteomics Laboratory, Barts Cancer Institute, Queen Mary University of London, London, United Kingdom.ORCID https://orcid.org/0000-0002-3426-2274
Esther Castellano SanchezTumour-Stroma Signalling Lab., Centro de Investigación del Cáncer, Instituto de Biología Molecular y Celular del Cáncer, Consejo Superior de Investigaciones Científicas (CSIC)-Universidad de Salamanca, Campus Miguel de Unamuno, Salamanca, Spain.ORCID https://orcid.org/0000-0002-8449-4081

Funding

Asociación Española Contra el Cáncer EPAEC222641CICSConsejo Superior de Investigaciones Científicas JAEICU-21-IBMCC-6CRUK Barts Centre Development FundJunta de Castilla y León CLC-2017-01Junta de Castilla y León CSI185-20Marie Curie PF7 MCA-ITN317445Ministerio de Ciencia e Innovación RTI2018-099161-A-I00
6 · The paper itself

Abstract

Macrophages are crucial in the body's inflammatory response, with tightly regulated functions for optimal immune system performance. Our study reveals that the RAS-p110α signalling pathway, known for its involvement in various biological processes and tumourigenesis, regulates two vital aspects of the inflammatory response in macrophages: the initial monocyte movement and later-stage lysosomal function. Disrupting this pathway, either in a mouse model or through drug intervention, hampers the inflammatory response, leading to delayed resolution and the development of more severe acute inflammatory reactions in live models. This discovery uncovers a previously unknown role of the p110α isoform in immune regulation within macrophages, offering insight into the complex mechanisms governing their function during inflammation and opening new avenues for modulating inflammatory responses.

Indexed as

Class I Phosphatidylinositol 3-KinasesInflammationMacrophagesras ProteinsSignal TransductionAnimalsDisease Models, AnimalLysosomesMiceMice, Inbred C57BLClass I Phosphatidylinositol 3-Kinasesras Proteinscell biologyimmunologyinflammationmacrophagesmouseRAS–p110α

Identifiers

PMID40272400
PMCPMC12021417

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.