Abstract
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.
Highlights
There is a need to advance our understanding of disease pathways that could provide new therapeutics to improve cardio-renal clinical outcomes
We showed that female G protein-coupled estrogen receptor 1 (GPER1) KO mice, but not males, have less ET-1, ETA, and ETB mRNA expression in kidney tissues [56]
Several studies suggest that GPER1 is responsible for acute estrogen-dependent vasodilation in both male and female rat aortas, which involved an increase in nitric oxide (NO) levels and a decrease in blood pressure [169–171] possibly through mediation of eNOS-dependent NO formation [164,167]
Summary
Cardiovascular (CV)-related events are the leading causes of mortality in the United. Renal disease is often both a cause and result of CV disease (CVD) [3] and is among the top 10 leading causes of death in the US and globally [1,2]. In 2020, heart disease was the leading cause of death in the US, accountable for. 696,962 deaths, and kidney disease was the tenth cause, responsible for 52,547 deaths out of. Despite the advanced therapies available, CV and renal disease remain increasingly prevalent, and the incidence of mortality from both continue to rise in the US and globally [4,5]. There is a need to advance our understanding of disease pathways that could provide new therapeutics to improve cardio-renal clinical outcomes
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