The activation of the G protein-coupled estrogen receptor (GPER) prevents and regresses cardiac hypertrophy

Mattía, Romina A. Di; Mariángelo, Juan Ignacio Elio; Blanco, Paula Graciela; Giusti, C; Portiansky, Enrique Leo; Mundiña‐Weilenmann, Cecilia; Aiello, Ernesto Alejandro; Orlowski, Alejandro

doi:10.1016/j.lfs.2019.117211

Cited by 13 publications

(12 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…• ↓ Cardiac hypertrophy (Azizian et al, 2018; Di Mattia et al, 2020; Jessup et al, 2010; Lenhart et al, 2013)…”

Section: Discussionmentioning

confidence: 99%

“…Men have a greater incidence of systolic heart failure than women. There is a growing body of preclinical evidence to suggest that GPER activation may improve some of the pathologies of heart failure, such as by reducing cardiac hypertrophy in males (Di Mattia et al, 2020; Lenhart et al, 2013), intact females (Jessup et al, 2010) and ovariectomised females (Azizian et al, 2018). Further supporting evidence comes from cardiomyocyte‐specific GPER‐deficient mice, which are reported to exhibit cardiac hypertrophy and impaired systolic and diastolic function (Wang, Sun, et al, 2017), as well as reduced fractional shortening and myocardial relaxation (Wang, Sun, et al, 2019).…”

Section: Gper and Outcomes Of Cardiovascular Eventsmentioning

confidence: 99%

See 1 more Smart Citation

G protein‐coupled estrogen receptor 1: a novel target to treat cardiovascular disease in a sex‐specific manner?

Dinh

Vinh

Drummond

et al. 2021

British J Pharmacology

View full text Add to dashboard Cite

As an agonist of the classical nuclear receptors, estrogen receptor‐α and ‐β (NR3A1/2), estrogen has been assumed to inhibit the development of cardiovascular disease in premenopausal women. Indeed, reduced levels of estrogen after menopause are believed to contribute to accelerated morbidity and mortality rates in women. However, estrogen replacement therapy has variable effects on cardiovascular risk in postmenopausal women, including increased serious adverse events. Interestingly, preclinical studies have shown that selective activation of the novel membrane‐associated G protein‐coupled estrogen receptor, GPER, can promote cardiovascular protection. These benefits are more evident in ovariectomised than intact females or in males. It is therefore possible that selective targeting of the GPER in postmenopausal women could provide cardiovascular protection with fewer adverse effects that are caused by conventional ‘receptor non‐specific’ estrogen replacement therapy. This review describes new data regarding the merits of targeting GPER to treat cardiovascular disease with a focus on sex differences.

show abstract

“…• ↓ Cardiac hypertrophy (Azizian et al, 2018; Di Mattia et al, 2020; Jessup et al, 2010; Lenhart et al, 2013)…”

Section: Discussionmentioning

confidence: 99%

Section: Gper and Outcomes Of Cardiovascular Eventsmentioning

confidence: 99%

G protein‐coupled estrogen receptor 1: a novel target to treat cardiovascular disease in a sex‐specific manner?

Dinh

Vinh

Drummond

et al. 2021

British J Pharmacology

View full text Add to dashboard Cite

show abstract

“…Previous studies have provided evidence for the cardioprotective role of GPER1 activation against heart failure in male mice [228] and myocardial inflammation in male SHR [76]. In addition, it was reported that GPER1 activation mitigates doxorubicin-induced cardiotoxicity in male rats, [191], protects against cardiomyocyte death [64,229], improves myocardial mechanical performance, and reduces infarct size in isolated rat and mouse hearts after ischemia reperfusion injury through the involvement of PI3K kinase/AKT signaling pathway [72,[230][231][232].…”

Section: Heart Diseasementioning

confidence: 98%

“…Furthermore, in vitro studies have shown no binding affinity for G-1 to estrogen receptors α or β (ERα and ERβ) [72,75]. G-1 modulates signaling pathways involved in the regulation of intracellular calcium [Ca 2+ ], phosphoinositide 3-kinase (PI3Ks), extracellular signal-related kinases (ERKs) and cyclic adenosine monophosphate (cAMP) [76,77]. GPER1 antagonists include G-15 and G-36 (Figure 2).…”

Section: Pharmacological and Genetic Tools To Study Gper1 Functionmentioning

confidence: 99%

Emerging Roles for G Protein-Coupled Estrogen Receptor 1 in Cardio-Renal Health: Implications for Aging

et al. 2022

View full text Add to dashboard Cite

Cardiovascular (CV) and renal diseases are increasingly prevalent in the United States and globally. CV-related mortality is the leading cause of death in the United States, while renal-related mortality is the 8th. Despite advanced therapeutics, both diseases persist, warranting continued exploration of disease mechanisms to develop novel therapeutics and advance clinical outcomes for cardio-renal health. CV and renal diseases increase with age, and there are sex differences evident in both the prevalence and progression of CV and renal disease. These age and sex differences seen in cardio-renal health implicate sex hormones as potentially important regulators to be studied. One such regulator is G protein-coupled estrogen receptor 1 (GPER1). GPER1 has been implicated in estrogen signaling and is expressed in a variety of tissues including the heart, vasculature, and kidney. GPER1 has been shown to be protective against CV and renal diseases in different experimental animal models. GPER1 actions involve multiple signaling pathways: interaction with aldosterone and endothelin-1 signaling, stimulation of the release of nitric oxide, and reduction in oxidative stress, inflammation, and immune infiltration. This review will discuss the current literature regarding GPER1 and cardio-renal health, particularly in the context of aging. Improving our understanding of GPER1-evoked mechanisms may reveal novel therapeutics aimed at improving cardio-renal health and clinical outcomes in the elderly.

show abstract

“…Moreover, G-1 regulation is involved in intracellular calcium [Ca2+] and phosphoadenosine 3-kinases (PI3Ks) signaling pathways. G-15 is a selective GPER1 antagonist with high binding affinity to GPER1 and less binding to ERα and ERβ [19,22,23]. As another selective GPER1 antagonist, G36 also owns poor binding ability to ERα and ERβ as well as G15, whereas G36 is more powerful than G15 in binding to GPER1 and then modulates Ca2+ mobilization and PI3K signaling [18].…”

Section: Gper Agonists and Antagonistsmentioning

confidence: 99%

The Research Advances in G-Protein-Coupled Estrogen Receptor

Zhang¹,

Wang²,

Wang³

2023

Estrogens - Recent Advances

View full text Add to dashboard Cite

Estrogen binds to the typical estrogen receptor (ER) ERα or ERβ and is translocated to the nucleus, where it binds directly to the estrogen response element of the target gene to induce transcription and regulate gene expression, and the whole process is completed in several hours to several days. The G protein-coupled estrogen receptor (GPER), a type that is structurally distinct from typical ERα and ERβ, rapidly induces most non-genomic effects within seconds to minutes. GPER regulates cell growth, migration, and programmed cell death in a variety of tissues and has been associated with the progression of estrogen-associated cancers. Here, the characteristics, cell signal transduction, and the latest research progress of GPER in estrogen-associated tumors and retinal diseases are reviewed.

show abstract

The activation of the G protein-coupled estrogen receptor (GPER) prevents and regresses cardiac hypertrophy

Cited by 13 publications

References 35 publications

G protein‐coupled estrogen receptor 1: a novel target to treat cardiovascular disease in a sex‐specific manner?

G protein‐coupled estrogen receptor 1: a novel target to treat cardiovascular disease in a sex‐specific manner?

Emerging Roles for G Protein-Coupled Estrogen Receptor 1 in Cardio-Renal Health: Implications for Aging

The Research Advances in G-Protein-Coupled Estrogen Receptor

Contact Info

Product

Resources

About