Evidence map›Paper›PMID 35128212›Full record

ReviewJACC. Basic to translational science2022

Targeting the Inflammasome in Cardiovascular Disease.

Maria Belland Olsen, Ida Gregersen, Øystein Sandanger, Kuan Yang, Marina Sokolova, Bente E Halvorsen, Lars Gullestad, Kaspar Broch, Pål Aukrust, Mieke C Louwe

Open access · goldAbstract readReview
In one paragraph

Review in JACC. Basic to translational science, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
97citing papers in PubMed, 3 pooled it
7.3field-weighted citation impact, top 2% of its field
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

97 citing papers in PubMed, 3 syntheses or guidelines pooled it, 155 citations in OpenAlex.

  1. Immunology of heart failure with preserved ejection fraction.Expert review of clinical immunology · 2025
    Pooled it
  2. Pooled it
  3. The Use of Sodium-Glucose Cotransporter-2 Inhibitors in Coronary Revascularization: Where Are We Now? A Systematic Review.American journal of cardiovascular drugs : drugs, devices, and other interventions · 2024
    Pooled it
  4. Trial
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  9. Repetitive pressure overload: species disparities, mechanisms, and translational relevance.American journal of physiology. Heart and circulatory physiology · 2026
    Article
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  11. Review
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37 more citing papers are in PubMed but not listed here.

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

10 authors at 2 institutions in 1 country.

Maria Belland OlsenResearch Institute of Internal Medicine, Oslo University Hospital, Oslo, Norway.
Ida GregersenResearch Institute of Internal Medicine, Oslo University Hospital, Oslo, Norway.
Øystein SandangerResearch Institute of Internal Medicine, Oslo University Hospital, Oslo, Norway.
Kuan YangResearch Institute of Internal Medicine, Oslo University Hospital, Oslo, Norway.
Marina SokolovaInstitute of Clinical Medicine, Faculty of Medicine, University of Oslo, Norway.
Bente E HalvorsenResearch Institute of Internal Medicine, Oslo University Hospital, Oslo, Norway.
Lars GullestadInstitute of Clinical Medicine, Faculty of Medicine, University of Oslo, Norway.
Kaspar BrochDepartment of Cardiology, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
Pål AukrustResearch Institute of Internal Medicine, Oslo University Hospital, Oslo, Norway.
Mieke C LouweResearch Institute of Internal Medicine, Oslo University Hospital, Oslo, Norway.
Oslo University Hospital · NOUniversity of Oslo · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The pathogenesis of cardiovascular disease (CVD) is complex and multifactorial, and inflammation plays a central role. Inflammasomes are multimeric protein complexes that are activated in a 2-step manner in response to infection or tissue damage. Upon activation the proinflammatory cytokines, interleukins-1β and -18 are released. In the last decade, the evidence that inflammasome activation plays an important role in CVD development became stronger. We discuss the role of different inflammasomes in the pathogenesis of CVD, focusing on atherosclerosis and heart failure. This review also provides an overview of existing experimental studies and clinical trials on inflammasome inhibition as a therapeutic target in these disorders.

Indexed as

ACS, acute coronary syndromeAIM2, absent in melanoma 2ASC, apoptosis associated speck-like proteinatherosclerosisATP, adenosine triphosphateCAD, coronary artery diseasecardiovascular diseaseCRP, C-reactive proteinCVD, cardiovascular diseaseDAMP, damage associated molecular patternGSDMD, gasdermin-DGSDMD-NT, gasdermin-D N-terminalheart failureHF, heart failureHFpEF, HF with preserved ejection fractionHFrEF, HF with reduced ejection fractionIL-1IL, interleukininflammasomeLDL, low-density lipoproteinLVEF, left ventricular ejection fractionLV, left ventricularMI, myocardial infarctionNF-κB, nuclear factor κBNLR, NOD-like receptorNLRP3NLRP3, NOD-like receptor family pyrin domain containing 3NOD, nucleotide-binding oligomerization domainPRR, pattern recognition receptorSTEMI, ST-elevation myocardial infarctionTLR, toll-like receptor

Identifiers

PMID35128212
PMCPMC8807732
OpenAlexW3208129514

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.