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


Journal

International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791

Informations de publication

Date de publication:
15 Jan 2022
Historique:
received: 05 01 2022
accepted: 14 01 2022
entrez: 21 1 2022
pubmed: 22 1 2022
medline: 5 2 2022
Statut: epublish

Résumé

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.

Identifiants

pubmed: 35055116
pii: ijms23020927
doi: 10.3390/ijms23020927
pmc: PMC8778295
pii:
doi:

Substances chimiques

AGTR1 protein, human 0
Autoantibodies 0
CXCL8 protein, human 0
IL6 protein, human 0
Interleukin-6 0
Interleukin-8 0
Reactive Oxygen Species 0
Receptor, Angiotensin, Type 1 0
Receptor, Endothelin A 0
TNF protein, human 0
Tumor Necrosis Factor-alpha 0
Collagen 9007-34-5

Types de publication

Journal Article Review

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : University of Padua
ID : BIRD2020_1

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Auteurs

Giovanni Civieri (G)

Department of Cardiac, Thoracic, Vascular Sciences and Public Health, University of Padova, 35128 Padova, Italy.

Laura Iop (L)

Department of Cardiac, Thoracic, Vascular Sciences and Public Health, University of Padova, 35128 Padova, Italy.

Francesco Tona (F)

Department of Cardiac, Thoracic, Vascular Sciences and Public Health, University of Padova, 35128 Padova, Italy.

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Classifications MeSH