Обзорная статья

The protective role of estrogen and estrogen receptors in cardiovascular disease and the controversial use of estrogen therapy

Andrea IorgaPresent address: Department of Medicine, Division of Gastroenterology/Liver, Keck School of Medicine of the University of Southern California, Los Angeles, CA, 90033, USAChristine M. CunninghamDepartment of Anesthesiology, Division of Molecular Medicine, David Geffen School of Medicine at University of California, Los Angeles, BH-160CHS, Los Angeles, CA, 90095-7115, USAShayan MoazeniDepartment of Anesthesiology, Division of Molecular Medicine, David Geffen School of Medicine at University of California, Los Angeles, BH-160CHS, Los Angeles, CA, 90095-7115, USAGrégoire RuffenachDepartment of Anesthesiology, Division of Molecular Medicine, David Geffen School of Medicine at University of California, Los Angeles, BH-160CHS, Los Angeles, CA, 90095-7115, USASoban UmarDepartment of Anesthesiology, Division of Molecular Medicine, David Geffen School of Medicine at University of California, Los Angeles, BH-160CHS, Los Angeles, CA, 90095-7115, USAMansoureh EghbaliDepartment of Anesthesiology, Division of Molecular Medicine, David Geffen School of Medicine at University of California, Los Angeles, BH-160CHS, Los Angeles, CA, 90095-7115, USA. [email protected]

2017en

ABI

Аннотация

Epidemiologic studies have previously suggested that premenopausal females have reduced incidence of cardiovascular disease (CVD) when compared to age-matched males, and the incidence and severity of CVD increases postmenopause. The lower incidence of cardiovascular disease in women during reproductive age is attributed at least in part to estrogen (E2). E2 binds to the traditional E2 receptors (ERs), estrogen receptor alpha (ERα), and estrogen receptor beta (ERβ), as well as the more recently identified G-protein-coupled ER (GPR30), and can exert both genomic and non-genomic actions. This review summarizes the protective role of E2 and its receptors in the cardiovascular system and discusses its underlying mechanisms with an emphasis on oxidative stress, fibrosis, angiogenesis, and vascular function. This review also presents the sexual dimorphic role of ERs in modulating E2 action in cardiovascular disease. The controversies surrounding the clinical use of exogenous E2 as a therapeutic agent for cardiovascular disease in women due to the possible risks of thrombotic events, cancers, and arrhythmia are also discussed. Endogenous local E2 biosynthesis from the conversion of testosterone to E2 via aromatase enzyme offers a novel therapeutic paradigm. Targeting specific ERs in the cardiovascular system may result in novel and possibly safer therapeutic options for cardiovascular protection.

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Идентификаторы

DOI: 10.1186/s13293-017-0152-8

Цитирования и источники

Цитирований: 2Использованных источников: 0

Показатели — AkademScholar