Evidence map›Paper›PMID 35055116›Full record

ReviewInternational journal of molecular sciences2022

Antibodies against Angiotensin II Type 1 and Endothelin 1 Type A Receptors in Cardiovascular Pathologies.

Giovanni Civieri, Laura Iop, Francesco Tona

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
6.1field-weighted citation impact, top 3% 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

29 citing papers in PubMed, 41 citations in OpenAlex.

  1. Review
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  10. Systemic sclerosis, main culprits and involved signaling pathways.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Review
  11. Review
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  17. Cardiac disease in systemic sclerosis: a narrative review.Archives of medical sciences. Atherosclerotic diseases · 2025
    Article
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  20. Observational
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 at 1 institution in 1 country.

Giovanni CivieriDepartment of Cardiac, Thoracic, Vascular Sciences and Public Health, University of Padova, 35128 Padova, Italy.ORCID 0000-0002-3076-4787
Laura IopDepartment of Cardiac, Thoracic, Vascular Sciences and Public Health, University of Padova, 35128 Padova, Italy.
Francesco TonaDepartment of Cardiac, Thoracic, Vascular Sciences and Public Health, University of Padova, 35128 Padova, Italy.ORCID 0000-0003-4828-7875
University of Padua · IT

Funding

University of Padua BIRD2020_1
6 · The paper itself

Abstract

Angiotensin II receptor type 1 (AT1R) and endothelin-1 receptor type A (ETAR) are G-protein-coupled receptors (GPCRs) expressed on the surface of a great variety of cells: immune cells, vascular smooth cells, endothelial cells, and fibroblasts express ETAR and AT1R, which are activated by endothelin 1 (ET1) and angiotensin II (AngII), respectively. Certain autoantibodies are specific for these receptors and can regulate their function, thus being known as functional autoantibodies. The function of these antibodies is similar to that of natural ligands, and it involves not only vasoconstriction, but also the secretion of proinflammatory cytokines (such as interleukin-6 (IL6), IL8 and TNF-α), collagen production by fibroblasts, and reactive oxygen species (ROS) release by fibroblasts and neutrophils. The role of autoantibodies against AT1R and ETAR (AT1R-AAs and ETAR-AAs, respectively) is well described in the pathogenesis of many medical conditions (e.g., systemic sclerosis (SSc) and SSc-associated pulmonary hypertension, cystic fibrosis, and allograft dysfunction), but their implications in cardiovascular diseases are still unclear. This review summarizes the current evidence regarding the effects of AT1R-AAs and ETAR-AAs in cardiovascular pathologies, highlighting their roles in heart transplantation and mechanical circulatory support, preeclampsia, and acute coronary syndromes.

Indexed as

AutoantibodiesCardiovascular DiseasesCollagenHumansInterleukin-6Interleukin-8Reactive Oxygen SpeciesReceptor, Angiotensin, Type 1Receptor, Endothelin ATumor Necrosis Factor-alphaAGTR1 protein, humanAutoantibodiesCollagenCXCL8 protein, humanIL6 protein, humanInterleukin-6Interleukin-8Reactive Oxygen SpeciesReceptor, Angiotensin, Type 1Receptor, Endothelin ATNF protein, humanTumor Necrosis Factor-alphaangiotensinAT1RautoantibodiescardiovascularcoronaryendothelinETARpreeclampsiareceptorstransplantation

Identifiers

PMID35055116
PMCPMC8778295
OpenAlexW4205560753

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.