ArticleInternational journal of biological sciences2019
G Protein-Coupled Estrogen Receptor 1 Inhibits Angiotensin II-Induced Cardiomyocyte Hypertrophy via the Regulation of PI3K-Akt-mTOR Signalling and Autophagy.
Article in International journal of biological sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 53 citations in OpenAlex.
- Cardiovascular risk in primary aldosteronism: inflammatory drivers, residual risk, and emerging combination strategies.Frontiers in endocrinology · 2026Review
- Qishen Huoxue Granule Ameliorates LPS-induced Cardiomyocyte Injury by Suppressing Excessive AutophagyCombinatorial chemistry & high throughput screening · 2026Article
- Pathogenic Role of mTOR Signaling in Cardiometabolic Disease: Implications for Heart, Liver, and Kidney Dysfunction.Physiological research · 2025Review
- Modeling the interplay of sex hormones in cardiac hypertrophic signaling.PLoS computational biology · 2025Article
- 17-beta estradiol prevents cardiac myocyte hypertrophy by regulating mitochondrial E3 ubiquitin ligase 1.Cell death & disease · 2025Article
- Bioinformatics analyses reveal the autophagy-related feature biomarkers in dilated cardiomyopathy with heart failure.Frontiers in cardiovascular medicine · 2025Article
- Autophagy fine-tuning by angiotensin-(1-9) in cultured rat cardiomyocytes.Frontiers in cardiovascular medicine · 2025Article
- The Estrogen-Autophagy Axis: Insights into Cytoprotection and Therapeutic Potential in Cancer and Infection.International journal of molecular sciences · 2024Review
- Engineered model of heart tissue repair for exploring fibrotic processes and therapeutic interventions.Nature communications · 2024Article
- Targeting estrogen receptor signaling for treating heart failure.Heart failure reviews · 2024Review
- S100A9 as a Key Myocardial Injury Factor Interacting with ATP5 Exacerbates Mitochondrial Dysfunction and Oxidative Stress in Sepsis-Induced Cardiomyopathy.Journal of inflammation research · 2024Article
- Advances in Research on the Effectiveness and Mechanism of Active Ingredients from Traditional Chinese Medicine in Regulating Hepatic Stellate Cells Autophagy Against Hepatic Fibrosis.Drug design, development and therapy · 2024Review
- Transforming growth factor-β and bone morphogenetic protein signaling pathways in pathological cardiac hypertrophy.Cell cycle (Georgetown, Tex.) · 2023Review
- Cardiac-specific Trim44 knockout in rat attenuates isoproterenol-induced cardiac remodeling via inhibition of AKT/mTOR pathway.Disease models & mechanisms · 2023Article
- The protective effect of Apelin-13 against cardiac hypertrophy through activating the PI3K-AKT-mTOR signaling pathway.Iranian journal of basic medical sciences · 2023Article
- The emerging role of estrogen's non-nuclear signaling in the cardiovascular disease.Frontiers in cardiovascular medicine · 2023Review
- Myotubularin-Related Protein14 Prevents Neointima Formation and Vascular Smooth Muscle Cell Proliferation by Inhibiting Polo-Like Kinase1.Journal of the American Heart Association · 2022Article
- Quantitative Proteomic Analysis of Zearalenone Exposure on Uterine Development in Weaned Gilts.Toxins · 2022Article
- The protective effects of 17-β estradiol and SIRT1 against cardiac hypertrophy: a review.Heart failure reviews · 2022Review
- Sexual dimorphism in cardiac remodeling: the molecular mechanisms ruled by sex hormones in the heart.Journal of molecular medicine (Berlin, Germany) · 2022Review
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Estrogen has been demonstrated to protect the heart against cardiac remodelling and heart failure in women. G protein-coupled estrogen receptor 1 (GPER1) is a recently discovered estrogen receptor (ER) that is expressed in various tissues. However, the mechanisms by which estrogen protects the heart, especially the roles played by ERs, are not clear. In this study, we explored the effect of GPER1 activation on angiotensin II (Ang II)-induced cardiomyocyte hypertrophy and the involved signalling pathways and mechanisms. Our data demonstrated that GPER1 is expressed in cardiomyocytes, a GPER1 agonist, G1, attenuated Ang II-induced cardiomyocyte hypertrophy and downregulated the mRNA expression levels of atrial natriuretic factor (ANF) and brain natriuretic peptide (BNP). Bioinformatics analysis revealed that five proteins, including RAP1gap, might be the key proteins involved in the attenuation of Ang II-induced cardiomyocyte hypertrophy by GPER1. G1 increased the protein level of p-Akt, p-70S6K1 and p-mTOR but decreased p-4EBP1 expression. All these effects were inhibited by either G15 (a GPER1 antagonist) or MK2206 (an inhibitor of Akt). Autophagy analysis showed that the LC3II/LC3I ratio was increased in Ang II-treated cells, and the increase was inhibited by G1 treatment. The effect of G1 on autophagy was blocked by treatment with G15, rapamycin, and MK2206. These results suggest that GPER1 activation attenuates Ang II-induced cardiomyocyte hypertrophy by upregulating the PI3K-Akt-mTOR signalling pathway and inhibiting autophagy.
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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 Socratic graph.