Evidence map›Paper›PMID 39969632›Full record

ReviewCurrent cardiology reports2025

Anti-inflammatory Therapies for Ischemic Heart Disease.

Tillmann Muhs, Senka Ljubojevic-Holzer, Susanne Sattler

Abstract readReview
In one paragraph

Review in Current cardiology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Article
  2. Observational
  3. Article
  4. Review
  5. 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

3 authors.

Tillmann MuhsDepartment of Pharmacology, Otto-Loewi Research Center, Medical University of Graz, Neue Stiftingtalstraße 6, 8010, Graz, Austria.
Senka Ljubojevic-HolzerDepartment of Cardiology, LKH Univ. Klinikum Graz, Medical University of Graz, Auenbruggerplatz 15, 8036, Graz, Austria.
Susanne SattlerDepartment of Pharmacology, Otto-Loewi Research Center, Medical University of Graz, Neue Stiftingtalstraße 6, 8010, Graz, Austria. s.sattler@imperial.ac.uk.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purpose of reviewThe inclusion of immunomodulatory strategies as supportive therapies in ischemic heart disease (IHD) has garnered significant support over recent years. Several such approaches appear to be unified through their ultimate target, the NLRP3 inflammasome. This review presents a brief update on immunomodulatory strategies in the continuum of conditions constituting ischemic heart disease and emphasising on the seemingly unifying mechanism of NLRP3 activation as well as modulation across these conditions. RECENT

findingsThe NLRP3 inflammasome is a multiprotein complex assembled upon inflammatory stimulation, causing the release of pro-inflammatory cytokines and initiating pyroptosis. The NLRP3 pathway is relevant in inflammatory signalling of cardiac immune cells as well as non-immune cells in the myocardium, including cardiomyocytes, fibroblasts and endothelial cells. In addition to a focus on clinical outcome and efficacy trials of targeting NLRP3-related pathways, the potential connection between immunomodulation in cardiology and the NLRP3 pathway is currently being explored in preclinical trials. Colchicine, cytokine-based approaches and SGLT2 inhibitors have emerged as promising agents. However, the conditions comprising IHD including atherosclerosis, coronary artery disease (CAD), myocardial infarction (MI) and ischemic cardiomyopathy/heart failure (iCMP/HF) are not equally amenable to immunomodulation with the respective drugs. Atherosclerosis, coronary artery disease and ischemic cardiomyopathy are affected by chronic inflammation, but the immunomodulatory approach to acute inflammation in the post-MI setting remains a pharmacological challenge, as detrimental and regenerative effects of myocardial inflammation are initiated in unison. The NLRP3 inflammasome lies at the center of cell mediated inflammation in IHD. Recent trial evidence has highlighted anti-inflammatory effects of colchicine, interleukin-based therapy as well as SGLT2i in IHD and that the respective drugs modulate the NLRP3 inflammasome.

Indexed as

Anti-Inflammatory AgentsMyocardial IschemiaNLR Family, Pyrin Domain-Containing 3 ProteinHumansInflammasomesInflammationAnti-Inflammatory AgentsInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, humanColchicineIL-6ImmunomodulationInflammationInterleukin therapyIschemic heart diseaseNLRP3 inflammasomeNLRP3 inhibitionSGLT2i

Identifiers

PMID39969632
PMCPMC11839821

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Registered trials

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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.