Evidence map›Paper›PMID 40956333›Full record

ArticleBasic research in cardiology2025

NLRP3 mediates lipid-driven macrophage proliferation in established atherosclerosis.

Carmen Härdtner, Felix Remmersmann, Carolin Ehlert, Christina Zehender, Tamara Antonela Vico, Bianca Dufner, Alexander von Ehr, Julia Hinterdobler, Xiaowei Li, Guido Pisani and 8 more

Abstract read
In one paragraph

Article in Basic research in cardiology, 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. Review
  2. Article
  3. Article
  4. Article
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

18 authors.

Carmen Härdtner *Department of Cardiology and Angiology, University Heart Center Freiburg-Bad Krozingen, Freiburg, Germany.
Felix Remmersmann *Department of Cardiology and Angiology, University Heart Center Freiburg-Bad Krozingen, Freiburg, Germany. felix.remmersmann@uniklinik-freiburg.de.ORCID 0009-0007-1462-9415
Carolin EhlertDepartment of Cardiology and Angiology, University Heart Center Freiburg-Bad Krozingen, Freiburg, Germany.
Christina ZehenderDepartment of Cardiology and Angiology, University Heart Center Freiburg-Bad Krozingen, Freiburg, Germany.
Tamara Antonela VicoDepartment of Cardiology and Angiology, University Heart Center Freiburg-Bad Krozingen, Freiburg, Germany.
Bianca DufnerDepartment of Cardiology and Angiology, University Heart Center Freiburg-Bad Krozingen, Freiburg, Germany.
Alexander von EhrDepartment of Cardiology and Angiology, University Heart Center Freiburg-Bad Krozingen, Freiburg, Germany.
Julia HinterdoblerDepartment of Cardiology, German Heart Center Munich, Technical University Munich, Lazarettstr. 36, 80636, Munich, Germany.
Xiaowei LiDepartment of Cardiology and Angiology, University Heart Center Freiburg-Bad Krozingen, Freiburg, Germany.
Guido PisaniDepartment of Cardiology and Angiology, University Heart Center Freiburg-Bad Krozingen, Freiburg, Germany.
Filip K SwirskiCardiovascular Research Institute, Cardiology, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Constantin von Zur MühlenDepartment of Cardiology and Angiology, University Heart Center Freiburg-Bad Krozingen, Freiburg, Germany.
Dennis WolfDepartment of Cardiology and Angiology, University Heart Center Freiburg-Bad Krozingen, Freiburg, Germany.
Martin CzernyDepartment of Cardiology and Angiology, University Heart Center Freiburg-Bad Krozingen, Freiburg, Germany.
Olaf GroßInstitute of Neuropathology, University Medical Center, University of Freiburg, Freiburg, Germany.
Hendrik B SagerDepartment of Cardiology, German Heart Center Munich, Technical University Munich, Lazarettstr. 36, 80636, Munich, Germany.
Dirk WestermannDepartment of Cardiology and Angiology, University Heart Center Freiburg-Bad Krozingen, Freiburg, Germany.
Ingo HilgendorfDepartment of Cardiology and Angiology, University Heart Center Freiburg-Bad Krozingen, Freiburg, Germany.

Funding

Deutsche Forschungsgemeinschaft HI1573/10Deutsche Forschungsgemeinschaft HI 1573/2; HI1573/9
6 · The paper itself

Abstract

An increased number of macrophages in the atherosclerotic plaque is associated with plaque instability and plaque progression. Lowering systemic cholesterol levels suppresses local macrophage proliferation and leads to plaque regression. However, the pathways regulating macrophage proliferation remain poorly understood. We investigated the cellular processes that underlie lipid-triggered local macrophage proliferation in the atherosclerotic plaque in transgenic mice and in human plaque tissue samples. Macrophages from mice with genetic deficiencies in scavenger receptors Cd36

Indexed as

AtherosclerosisCell ProliferationLipid MetabolismMacrophagesNLR Family, Pyrin Domain-Containing 3 ProteinPlaque, AtheroscleroticAnimalsApoptosisATP Binding Cassette Transporter 1ATP Binding Cassette Transporter, Subfamily G, Member 1CD36 AntigensDisease Models, AnimalHumansInflammasomesMaleMiceAbca1 protein, mouseABCG1 protein, mouseATP Binding Cassette Transporter 1ATP Binding Cassette Transporter, Subfamily G, Member 1CD36 AntigensCd36 protein, mouseInflammasomesMsr1 protein, mouseNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseScavenger Receptors, Class AAtherosclerosisMacrophagesMCC950NLRP3Proliferation

Identifiers

PMID40956333
PMCPMC12680701

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.