Evidence map›Paper›PMID 40787764›Full record

ArticleESC heart failure2025

Multiorgan characterization of inflammasome component expression in a rat model of advanced heart failure.

Dávid Nagy, Zsófia Onódi, Márton Kocsis, Artúr Tóth, Tímea Bálint, Attila Oláh, Alex Ali Sayour, Bálint András Barta, Béla Merkely, Péter Ferdinandy and 3 more

Abstract read
In one paragraph

Article in ESC heart failure, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. 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

13 authors.

Dávid NagyDepartment of Cardiology, Heart and Vascular Center, Semmelweis University, Budapest, Hungary.
Zsófia OnódiDepartment of Pharmacology and Pharmacotherapy, Center for Pharmacology and Drug Research and Development, Semmelweis University, Budapest, Hungary.
Márton KocsisDepartment of Pharmacology and Pharmacotherapy, Center for Pharmacology and Drug Research and Development, Semmelweis University, Budapest, Hungary.
Artúr TóthDepartment of Pharmacology and Pharmacotherapy, Center for Pharmacology and Drug Research and Development, Semmelweis University, Budapest, Hungary.
Tímea BálintDepartment of Cardiology, Heart and Vascular Center, Semmelweis University, Budapest, Hungary.
Attila OláhDepartment of Cardiology, Heart and Vascular Center, Semmelweis University, Budapest, Hungary.
Alex Ali SayourDepartment of Cardiology, Heart and Vascular Center, Semmelweis University, Budapest, Hungary.
Bálint András BartaDepartment of Cardiology, Heart and Vascular Center, Semmelweis University, Budapest, Hungary.
Béla MerkelyDepartment of Cardiology, Heart and Vascular Center, Semmelweis University, Budapest, Hungary.
Péter FerdinandyDepartment of Pharmacology and Pharmacotherapy, Center for Pharmacology and Drug Research and Development, Semmelweis University, Budapest, Hungary.
Tamás RadovitsDepartment of Cardiology, Heart and Vascular Center, Semmelweis University, Budapest, Hungary.
Zoltán V VargaDepartment of Pharmacology and Pharmacotherapy, Center for Pharmacology and Drug Research and Development, Semmelweis University, Budapest, Hungary.
Mihály RuppertDepartment of Cardiology, Heart and Vascular Center, Semmelweis University, Budapest, Hungary.

Funding

European Union 739593European Union LP-2021-14European Union RRF-2.3.1-21-2022-00003János Bolyai Research Scholarship of the Hungarian Academy of Sciences BO/00012/24/5János Bolyai Research Scholarship of the Hungarian Academy of Sciences BO/00619/22Ministry of Innovation and Technology of Hungary from the National Research, Development and Innovation Fund TKP2021-EGA-23National Research, Development and Innovation Fund EKÖP-2024-18National Research, Development and Innovation Office (NKFIH) of Hungary ADVANCED 150829National Research, Development and Innovation Office (NKFIH) of Hungary FK134751National Research, Development and Innovation Office (NKFIH) of Hungary K134939National Research, Development and Innovation Office (NKFIH) of Hungary STARTING150923New National Excellence Program of the Ministry for Innovation and Technology from the National Research, Development and Innovation Fund ÚNKP-22-3-I-SE-7New National Excellence Program of the Ministry for Innovation and Technology from the National Research, Development and Innovation Fund ÚNKP-23-4-II-SE-26
6 · The paper itself

Abstract

aimsTargeting inflammasomes in heart failure (HF) might represent a novel therapeutic option. Nevertheless, previous studies focused only on myocardial inflammasome alterations, and data are scarce regarding their regulation and role in HF-associated multiorgan dysfunction. Therefore, we aimed to determine the myocardial, pulmonary, hepatic and renal expression of various inflammasome components in a rat model of advanced HF. METHODS AND

resultsRats underwent transverse aortic constriction (TAC) and were followed-up for 15 weeks. Animals featuring two to three clinical signs of advanced HF were included in the TAC-HF group (n = 6). TAC rats with mild HF were also investigated (0-1 signs, TAC-M group, n = 6). Six sham-operated animals served as controls. The expressions of inflammasome component proteins in left ventricle (LV), right ventricle (RV), lung, liver and kidney tissue were measured with Western blot. Despite the differences between the clinical state of the TAC-HF and TAC-M groups, severe cardiac dysfunction and myocardial remodelling developed in all TAC animals. Absent in melanoma 2 (AIM2) and NLR family CARD domain-containing protein 4 (NLRC4) inflammasome sensors were up-regulated in both the LV and RV of the TAC-HF group compared with sham. AIM2 and NLR family pyrin domain-containing protein 3 (NLRP3), but not NLRC4 expression were elevated in the lungs of the TAC-HF animals. Additionally, pulmonary congestion and CD68-positive leukocyte infiltration were observed in both TAC groups. Inflammasome components were down-regulated in the liver and remained unchanged in the kidneys of the TAC-HF group, despite the presence of renal atrophy and fibrosis. Inflammasome changes were predominantly absent in TAC-M animals.

conclusionsInflammasome expression shows distinct patterns in specific organs in advanced HF. Future studies aiming to antagonize inflammation in HF should take these findings into consideration.

Indexed as

Heart FailureHeart VentriclesInflammasomesLungMyocardiumAnimalsBlotting, WesternCalcium-Binding ProteinsDisease Models, AnimalKidneyLiverMaleRatsRats, Sprague-DawleyVentricular RemodelingCalcium-Binding ProteinsInflammasomesAbsent in melanoma 2Advanced heart failureEnd‐organ damageInflammasomeNLR family CARD domain‐containing protein 4NLR family pyrin domain‐containing protein 3

Identifiers

PMID40787764
PMCPMC12450780

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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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 Socratic graph.