Evidence map›Paper›PMID 41828478›Full record

ArticleInternational journal of molecular sciences2026

Transcriptional Remodeling of Microglia After Experimental Myocardial Infarction.

Jan Traub, Nico Hofmann, Clément Cochain, Giuseppe Rizzo, Antoine-Emmanuel Saliba, Tobias Krammer, Stefan Frantz, Ulrich Hofmann, Katrin Sinning, Martin Vaeth and 1 more

Abstract read
In one paragraph

Article in International journal of molecular sciences, 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

11 authors.

Jan TraubDepartment of Internal Medicine I, University Hospital Würzburg, 97080 Wuerzburg, Germany.ORCID 0000-0001-8092-5967
Nico HofmannDepartment of Internal Medicine I, University Hospital Würzburg, 97080 Wuerzburg, Germany.
Clément CochainInstitute of Experimental Biomedicine, Department of Experimental Biomedicine I, University Hospital Würzburg, 97080 Wuerzburg, Germany.
Giuseppe RizzoInstitute of Experimental Biomedicine, Department of Experimental Biomedicine I, University Hospital Würzburg, 97080 Wuerzburg, Germany.ORCID 0009-0008-5366-0738
Antoine-Emmanuel SalibaHelmholtz Institute for RNA-Based Infection Research, Helmholtz Centre for Infection Research, 97080 Wuerzburg, Germany.ORCID 0000-0001-8539-2784
Tobias KrammerHelmholtz Institute for RNA-Based Infection Research, Helmholtz Centre for Infection Research, 97080 Wuerzburg, Germany.
Stefan FrantzDepartment of Internal Medicine I, University Hospital Würzburg, 97080 Wuerzburg, Germany.
Ulrich HofmannDepartment of Internal Medicine I, University Hospital Würzburg, 97080 Wuerzburg, Germany.ORCID 0000-0002-3681-2073
Katrin SinningMax Planck Research Group, Würzburg Institute of Systems Immunology, University of Würzburg, 97080 Wuerzburg, Germany.ORCID 0009-0004-5841-2398
Martin VaethMax Planck Research Group, Würzburg Institute of Systems Immunology, University of Würzburg, 97080 Wuerzburg, Germany.
Anna FreyDepartment of Internal Medicine I, University Hospital Würzburg, 97080 Wuerzburg, Germany.ORCID 0000-0002-2955-6753

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Beyond cardiac impairment, myocardial infarction (MI) affects the central nervous system (CNS), where it has been associated with neuroinflammation and cognitive dysfunction. Microglia, the resident immune cells of the CNS, are key regulators of neuroinflammatory processes. However, the transcriptional landscape of microglia following MI remains incompletely understood. We hypothesized that MI induces transcriptional remodeling in microglia that may reflect altered metabolic regulation. Male C57BL/6J mice underwent permanent LAD ligation or sham surgery. Five days post-MI, CD45-intermediate and SiglecH/CD11b-positive immune cells were isolated from cortical and subcortical regions by FACS and subjected to single-cell RNA sequencing. Complementary exploratory metabolic assays included assessment of mitochondrial mass and membrane potential as well as glucose uptake. Microglia represented the predominant immune cell population in both the cortex and subcortex. Subclustering revealed a significantly increased proportion of a "low translational" microglial subset after MI. Pseudobulk differential expression and gene set enrichment analyses demonstrated significant downregulation of translation-related pathways in cortical microglia and proteostasis-associated pathways in subcortical microglia. These transcriptional changes were accompanied by a significant reduction in mitochondrial mass and metabolic observations consistent with altered energetic regulation, although several functional readouts did not reach statistical significance. Experimental MI is associated with region-specific transcriptional remodeling of microglia, characterized by reduced expression of energy-intensive and proteostasis-related pathways. Exploratory metabolic observations are consistent with altered energetic regulation but require confirmation in adequately powered studies. These findings suggest that systemic cardiac injury is linked to microglial transcriptional adaptation in the early post-infarction phase.

Indexed as

MicrogliaMyocardial InfarctionTranscription, GeneticAnimalsDisease Models, AnimalGene Expression ProfilingGene Expression RegulationMaleMiceMice, Inbred C57BLMitochondriaTranscriptomeCNSmetabolismmicrogliamyocardial infarctionneuroinflammation

Identifiers

PMID41828478
PMCPMC12986541

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.