ArticleInternational journal of endocrinology2021
G Protein-Coupled Estrogen Receptor 1 (GPER1) Mediates Aldosterone-Induced Endothelial Inflammation in a Mineralocorticoid Receptor-Independent Manner.
Article in International journal of endocrinology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- Aldosterone-mineralocorticoid receptor interactions: new insights and therapeutic perspectives in primary aldosteronism.Hypertension research : official journal of the Japanese Society of Hypertension · 2026Review
- Cardiovascular risk in primary aldosteronism: inflammatory drivers, residual risk, and emerging combination strategies.Frontiers in endocrinology · 2026Review
- Article
- Interaction of GPER-1 with the endocrine signaling axis in breast cancer.Frontiers in endocrinology · 2025Review
- The role of sex hormones in aldosterone biosynthesis and their potential impact on its mineralocorticoid receptor.Cardiovascular endocrinology & metabolism · 2024Review
- G-Protein Coupled Receptor 1 Is Involved in Tetrachlorobisphenol A-Induced Inflammatory Response in Jurkat Cells.Toxics · 2024Article
- G protein-coupled estrogen receptor: a promising therapeutic target for aldosterone-induced hypertension.Frontiers in endocrinology · 2023Review
- Emerging vascular cell-specific roles for mineralocorticoid receptor: implications for understanding sex differences in cardiovascular disease.American journal of physiology. Cell physiology · 2023Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveIt has been increasingly appreciated that G protein-coupled estrogen receptor 1 (GPER1) mediates both proinflammatory and anti-inflammatory response of estrogen. It is also involved in some rapid vascular effects of aldosterone in a mineralocorticoid receptor (MR) independent manner. However, whether GPER1 mediates aldosterone-induced inflammation response in endothelial cells and its relationship with MR are yet undetermined and therefore require further explanation.
methodBased on the hypothesis that GPER1 plays a role in the aldosterone-related vascular inflammation, the present study utilized a model of human umbilical vein endothelial cells transfected with MR siRNA and induced for inflammatory response with increasing concentration of aldosterone.
resultsIt was discovered that induction of aldosterone had no effect on the expression of GPER1 but promoted the expression of MR. Suppression of MR did not influence GPER1 expression, and GPER1 was capable of mediating part of aldosterone-induced endothelial inflammatory response. This effect may involve phosphoinositide 3-kinases (PI3K) pathway signaling.
conclusionThese findings not only demonstrated the role of GPER1 in aldosterone-induced vascular inflammation but also suggested an alternative for pharmaceutical treatment of hyperaldosteronism considering the unsatisfying effect on cardiovascular risks with MR antagonists.
Identifiers
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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.