Evidence map›Paper›PMID 35867264›Full record

ArticleInflammation2022

Angiotensin II Triggers NLRP3 Inflammasome Activation by a Ca

Jenaro Antonio Espitia-Corredor, Pía Boza, Claudio Espinoza-Pérez, José Miguel Lillo, Constanza Rimassa-Taré, Víctor Machuca, José Miguel Osorio-Sandoval, Raúl Vivar, Samir Bolivar, Viviana Pardo-Jiménez and 3 more

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

19 citing papers in PubMed, 28 citations in OpenAlex.

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  9. Animal and cellular models of atrial fibrillation: a review.Frontiers in cardiovascular medicine · 2025
    Review
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  17. Loss of IP3R-BKInternational journal of molecular sciences · 2023
    Article
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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 at 4 institutions in 3 countries.

Jenaro Antonio Espitia-Corredor *Laboratory of Molecular Pharmacology, Faculty of Chemical and Pharmaceutical Sciences, Department of Pharmacological & Toxicological Chemistry, University of Chile, Santiago, Chile.
Pía Boza *Laboratory of Molecular Pharmacology, Faculty of Chemical and Pharmaceutical Sciences, Department of Pharmacological & Toxicological Chemistry, University of Chile, Santiago, Chile.
Claudio Espinoza-PérezLaboratory of Molecular Pharmacology, Faculty of Chemical and Pharmaceutical Sciences, Department of Pharmacological & Toxicological Chemistry, University of Chile, Santiago, Chile.
José Miguel LilloLaboratory of Molecular Pharmacology, Faculty of Chemical and Pharmaceutical Sciences, Department of Pharmacological & Toxicological Chemistry, University of Chile, Santiago, Chile.
Constanza Rimassa-TaréLaboratory of Molecular Pharmacology, Faculty of Chemical and Pharmaceutical Sciences, Department of Pharmacological & Toxicological Chemistry, University of Chile, Santiago, Chile.
Víctor MachucaLaboratory of Molecular Pharmacology, Faculty of Chemical and Pharmaceutical Sciences, Department of Pharmacological & Toxicological Chemistry, University of Chile, Santiago, Chile.
José Miguel Osorio-SandovalLaboratory of Molecular Pharmacology, Faculty of Chemical and Pharmaceutical Sciences, Department of Pharmacological & Toxicological Chemistry, University of Chile, Santiago, Chile.
Raúl VivarMolecular and Clinical Pharmacology Program, Faculty of Medicine, Institute of Biomedical Sciences (ICBM), University of Chile, Santiago, Chile.
Samir BolivarFaculty of Chemistry and Pharmacy, Universidad del Atlántico, Barranquilla, Colombia.
Viviana Pardo-JiménezLaboratory of Molecular Pharmacology, Faculty of Chemical and Pharmaceutical Sciences, Department of Pharmacological & Toxicological Chemistry, University of Chile, Santiago, Chile.
Carlos Félix Sánchez-FerrerFaculty of Medicine, Department of Pharmacology, Universidad Autónoma de Madrid, Madrid, Spain.
Concepción PeiróFaculty of Medicine, Department of Pharmacology, Universidad Autónoma de Madrid, Madrid, Spain.
Guillermo Díaz-ArayaLaboratory of Molecular Pharmacology, Faculty of Chemical and Pharmaceutical Sciences, Department of Pharmacological & Toxicological Chemistry, University of Chile, Santiago, Chile. gadiaz@ciq.uchile.cl.ORCID http://orcid.org/0000-0001-7960-8104
University of Chile · CLAdvanced Center for Chronic Diseases · CLHospital La Paz Institute for Health Research · ESUniversity of Atlántico · CO

Funding

Comisión Nacional de Investigación Científica y Tecnológica FONDAP ACCDiS grant 15130011Fondo de Fomento al Desarrollo Científico y Tecnológico FONDECYT 1170425Fondo de Fomento al Desarrollo Científico y Tecnológico FONDECYT 1210627
6 · The paper itself

Abstract

Angiotensin II (Ang-II) is a widely studied hypertensive, profibrotic, and pro-inflammatory peptide. In the heart, cardiac fibroblasts (CF) express type 1 angiotensin II receptors (AT1R), Toll-like receptor-4 (TLR4), and the NLRP3 inflammasome complex, which play important roles in pro-inflammatory processes. When activated, the NLRP3 inflammasome triggers proteolytic cleavage of pro-IL-1, resulting in its activation. However, in CF the mechanism by which Ang-II assembles and activates the NLRP3 inflammasome remains not fully known. To elucidate this important point, we stimulated TLR4 receptors in CF and evaluated the signaling pathways by which Ang-II triggers the assembly and activity. In cultured rat CF, pro-IL-1β levels, NLRP3, ASC, and caspase-1 expression levels were determined by Western blot. NLRP3 inflammasome complex assembly was analyzed by immunocytochemistry, whereas by ELISA, we analyzed NLRP3 inflammasome activity and [Formula: see text] release. In CF, Ang-II triggered NLRP3 inflammasome assembly and caspase-1 activity; and in LPS-pretreated CF, Ang-II also triggered [Formula: see text] secretion. These effects were blocked by losartan (AT1R antagonist), U73221 (PLC inhibitor), 2-APB (IP3R antagonist), and BAPTA-AM (Ca

Indexed as

InflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinAngiotensin IIAnimalsCaspase 1FibroblastsInterleukin-1betaRatsToll-Like Receptor 4Angiotensin IICaspase 1InflammasomesInterleukin-1betaNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, ratToll-Like Receptor 4Angiotensin IICardiac fibroblastsIL-1β secretionNLRP3 inflammasome

Identifiers

PMID35867264
OpenAlexW4286697496

What OpenQuestion holds

Textmetadata
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.