ArticleLife sciences2016
GPER is required for the age-dependent upregulation of the myocardial endothelin system.
Article in Life sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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The trial behind it
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Short-term estradiol administration does not restore endothelin-B receptor-mediated vasodilation in postmenopausal women.American journal of physiology. Heart and circulatory physiology · 2025Article
- Endothelin receptor B is required for the blood pressure-lowering effect of G protein-coupled estrogen receptor 1 in ovariectomized rats.American journal of physiology. Renal physiology · 2024Article
- The G protein-coupled oestrogen receptor GPER in health and disease: an update.Nature reviews. Endocrinology · 2023Review
- Emerging Roles for G Protein-Coupled Estrogen Receptor 1 in Cardio-Renal Health: Implications for Aging.Biomolecules · 2022Review
- Advances in the study of nicotinamide adenine dinucleotide phosphate oxidase in myocardial remodeling.Frontiers in cardiovascular medicine · 2022Review
- Article
- Evidence for G-Protein-Coupled Estrogen Receptor as a Pronatriuretic Factor.Journal of the American Heart Association · 2020Article
- Nox1 downregulators: A new class of therapeutics.Steroids · 2019Review
- GPCRs in context: sexual dimorphism in the cardiovascular system.British journal of pharmacology · 2018Review
- Twenty years of the G protein-coupled estrogen receptor GPER: Historical and personal perspectives.The Journal of steroid biochemistry and molecular biology · 2018Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
aimsCardiac aging is associated with progressive structural changes and functional impairment, such as left ventricular hypertrophy, fibrosis and diastolic dysfunction. Aging also increases myocardial activity of endothelin-1 (ET-1), a multifunctional peptide with growth-promoting and pro-fibrotic activity. Because the G protein-coupled estrogen receptor (GPER) regulates vascular responsiveness to ET-1, we investigated whether GPER also plays a role in the regulation of the myocardial endothelin system with aging. MAIN
methodsYoung (4month-old) and aged (24month-old) wild-type and Gper-deficient (Gper(-/-)) mice were studied. Gene expression levels of prepro-ET-1, endothelin converting enzymes ECE-1 and ECE-2, and endothelin ETA and ETB receptors were determined by qPCR in left ventricular myocardium. KEY
findingsAging markedly increased steady-state mRNA expression levels of ECE-1, ECE-2, ETA and ETB receptors (each p<0.001 vs. young mice). Deletion of Gper inhibited the age-dependent increase in ECE-2 and ETB receptor mRNA levels (57% and 40% reduction, respectively, each p<0.01 vs. wild-type mice), whereas gene expression of prepro-ET-1, ECE-1, and the ETA receptor was unaffected in Gper(-/-) mice. SIGNIFICANCE: We identified a novel regulatory mechanism through which the endogenous Gper facilitates the age-dependent increase in myocardial expression of ECE-2 and the ETB receptor, which is compatible with an activating role of GPER for the local endothelin system with aging. Targeting GPER signaling by selective antagonists may therefore be considered a new therapeutic approach to reduce age-dependent increased ET-1 activity and the associated development of left ventricular hypertrophy, fibrosis and heart failure.
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Registered trials
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.