Evidence map›Paper›PMID 41677605›Full record

ArticleCells2026

Irf5 Knockdown in Bone Marrow-Derived Macrophages Favors M1-to-M2 Transition.

Elizaveta Petrova, Ekaterina Sherstyukova, Snezhanna Kandrashina, Vladimir Inozemtsev, Alexandra Tsitrina, Viktoriya Fedorova, Mikhail Shvedov, Artem Kuzovlev, Maxim Dokukin, Yuri Kotelevtsev and 2 more

Abstract read
In one paragraph

Article in Cells, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. The role of IRF5 as an immune regulator.Biochemical Society transactions · 2026
    Review
  2. Review
  3. 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

12 authors.

Elizaveta PetrovaOdintsovo Center of Medical and Biological Technologies, 143025 Moscow, Russia.
Ekaterina SherstyukovaFederal Research and Clinical Center of Intensive Care Medicine and Rehabilitology, V.A. Negovsky Research Institute of General Reanimatology, 107031 Moscow, Russia.ORCID 0000-0002-9962-6315
Snezhanna KandrashinaFederal Research and Clinical Center of Intensive Care Medicine and Rehabilitology, V.A. Negovsky Research Institute of General Reanimatology, 107031 Moscow, Russia.ORCID 0000-0002-2185-3817
Vladimir InozemtsevFederal Research and Clinical Center of Intensive Care Medicine and Rehabilitology, V.A. Negovsky Research Institute of General Reanimatology, 107031 Moscow, Russia.ORCID 0000-0002-4693-5624
Alexandra TsitrinaIlse Katz Institute for Nanoscale Science and Technology, Ben-Gurion University of the Negev, Beer Sheva 8410501, Israel.ORCID 0000-0002-2827-9993
Viktoriya FedorovaOdintsovo Center of Medical and Biological Technologies, 143025 Moscow, Russia.ORCID 0009-0000-0600-0827
Mikhail ShvedovFederal Research and Clinical Center of Intensive Care Medicine and Rehabilitology, V.A. Negovsky Research Institute of General Reanimatology, 107031 Moscow, Russia.ORCID 0009-0004-4288-2758
Artem KuzovlevFederal Research and Clinical Center of Intensive Care Medicine and Rehabilitology, V.A. Negovsky Research Institute of General Reanimatology, 107031 Moscow, Russia.
Maxim DokukinFederal Research and Clinical Center of Intensive Care Medicine and Rehabilitology, V.A. Negovsky Research Institute of General Reanimatology, 107031 Moscow, Russia.ORCID 0000-0001-6856-1953
Yuri KotelevtsevOdintsovo Center of Medical and Biological Technologies, 143025 Moscow, Russia.ORCID 0000-0002-7255-7794
Arsen MikaelyanKoltzov Institute of Developmental Biology of the Russian Academy of Sciences, 26 Vavilov Street, 119334 Moscow, Russia.ORCID 0000-0003-4358-2357
Viktoria SergunovaFederal Research and Clinical Center of Intensive Care Medicine and Rehabilitology, V.A. Negovsky Research Institute of General Reanimatology, 107031 Moscow, Russia.ORCID 0000-0002-8425-0845

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The transcription factor IRF5 maintains macrophages in the pro-inflammatory M1 state. We assessed the effects of siRNA-mediated knockdown of Irf5 on murine bone marrow-derived macrophages (BMDM) in M0, M1 and M2 states. Knockdown of Irf5 in M1 macrophages made them phenotypically similar to M2 macrophages, which was reflected in the decreased expression of the M1 marker iNOS, increased expression of the M2 marker CD206, increased mitochondrial content and respective morphological changes. Interestingly, the M2 phenotype was also affected by the reduction in Irf5. Using atomic force microscopy (AFM), we showed that Irf5 knockdown increases plasma membrane roughness, particularly in M2 macrophages. AFM-based stiffness measurements indicated that Irf5 knockdown altered macrophage elasticity, potentially influencing their functional behavior. Our data suggest a complex role of IRF5 in macrophage polarization, supporting its dual role as a transcriptional activator and repressor both in M1 and M2 states, and highlight the importance of IRF5 in the maintenance of metabolic and functional properties of macrophages.

Indexed as

Bone Marrow CellsGene Knockdown TechniquesInterferon Regulatory FactorsMacrophagesAnimalsCell DifferentiationCell MembraneLectins, C-TypeMannose-Binding LectinsMannose ReceptorMiceMice, Inbred C57BLMicroscopy, Atomic ForceMitochondriaRNA, Small InterferingInterferon Regulatory FactorsIrf5 protein, mouseLectins, C-TypeMannose-Binding LectinsMannose ReceptorRNA, Small Interferingatomic force microscopybiomechanicsIRF5M1M2macrophagesmitochondriapolarizationsiRNAYoung’s modulus

Identifiers

PMID41677605
PMCPMC12897094

What OpenQuestion holds

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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.