Evidence map›Paper›PMID 34098096›Full record

ArticleVascular pharmacology2021

Angiotensin-II activates vascular inflammasome and induces vascular damage.

Stefany B Cau, Ariane Bruder-Nascimento, Marcondes B Silva, Fernanda N Z Ramalho, Fabiola Mestriner, Rheure Alves-Lopes, Nathanne Ferreira, Rita C Tostes, Thiago Bruder-Nascimento

Open access · greenAbstract read
In one paragraph

Article in Vascular pharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 13% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.

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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

9 authors at 3 institutions in 2 countries.

Stefany B CauDepartment of Pharmacology, Ribeirao Preto Medical School, University of Sao Paulo, Brazil; Department of Pharmacology, Institute of Biological Sciences, Federal University of Minas Gerais, Brazil.
Ariane Bruder-NascimentoDepartment of Pediatrics, University of Pittsburgh, USA; Center for Pediatric Research in Obesity & Metabolism (CPROM), University of Pittsburgh, USA.
Marcondes B SilvaDepartment of Pharmacology, Ribeirao Preto Medical School, University of Sao Paulo, Brazil.
Fernanda N Z RamalhoDepartment of Pharmacology, Ribeirao Preto Medical School, University of Sao Paulo, Brazil.
Fabiola MestrinerDepartment of Pharmacology, Ribeirao Preto Medical School, University of Sao Paulo, Brazil.
Rheure Alves-LopesDepartment of Pharmacology, Ribeirao Preto Medical School, University of Sao Paulo, Brazil.
Nathanne FerreiraDepartment of Pharmacology, Ribeirao Preto Medical School, University of Sao Paulo, Brazil.
Rita C TostesDepartment of Pharmacology, Ribeirao Preto Medical School, University of Sao Paulo, Brazil.
Thiago Bruder-NascimentoDepartment of Pharmacology, Ribeirao Preto Medical School, University of Sao Paulo, Brazil; Department of Pediatrics, University of Pittsburgh, USA; Center for Pediatric Research in Obesity & Metabolism (CPROM), University of Pittsburgh, USA; Vascular Medicine Institute (VMI), University of Pittsburgh, USA. Electronic address: bruder@pitt.edu.
Universidade de São Paulo · BRUniversidade Federal de Minas Gerais · BRUniversity of Pittsburgh · US

Funding

Leptin, a therapeutic avenue for the treatment of vascular disease, focus on congenital and antiretroviral therapy-associated lipodystrophiesR00HL140139 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI BRUDER, THIAGO · 2019 to 2021
$733k
NHLBI NIH HHS R00 HL140139
6 · The paper itself

Abstract

Angiotensin-II (Ang-II), a major target for treatment of cardiovascular disease, promotes cardiovascular dysfunction by directly modulating structure and function of vascular cells. Inflammasome components are expressed in the vasculature and are activated by specific stimuli. However, whether Ang-II activates the inflammasome in vascular cells or inflammasome activation contributes to Ang-II-induced vascular damage is still not fully elucidated. We tested the hypothesis that Ang-II induces endothelial dysfunction, vascular remodeling, and high blood pressure via inflammasome activation. C57BL6/J wild type (WT) and Caspase-1 knockout (Casp1-/-) mice were infused with vehicle or Ang-II for two weeks (490 ng/Kg/day) to determine whether the inflammasome contributes to vascular damage induced by Ang-II. Rat Aortic Vascular Smooth Muscle cells (RASMC) were used to determine if the interaction between Ang-II and inflammasomes causes migration and proliferation of vascular smooth muscle cells. Ex vivo studies revealed that Ang-II infusion induced vascular oxidative stress, endothelial dysfunction and vascular remodeling in WT mice. Casp1-/- mice were protected against Ang-II-induced vascular injury. In vitro experiments, Ang-II activated the NLRP3 inflammasome in RASMC, i.e. Ang-II increased Caspase-1 (Casp1) activity and cleavage of pro-interleukin (IL)-1β. MCC950 (NLRP3 receptor antagonist) prevented Ang-II-induced vascular migration and proliferation, but failed to reduce reactive oxygen species production. In conclusion, Ang-II leads to inflammasome activation in the vasculature contributing to endothelial dysfunction and vascular remodeling. Taken together, we place inflammasomes as a possible therapeutic target in conditions associated with increased Ang-II levels.

Indexed as

Angiotensin IIInflammasomesAnimalsCells, CulturedMiceMice, Inbred C57BLMice, KnockoutNLR Family, Pyrin Domain-Containing 3 ProteinRatsAngiotensin IIInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinAngiotensin-IIInflammasomeVascular damage

Identifiers

PMID34098096
PMCPMC8569482
OpenAlexW3170572215

What OpenQuestion holds

Textmetadata
LicenceTDM
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.