Estrogen-mediated protection against coronary heart disease: The role of the Notch pathway. Issue 189 (May 2019)

• Record Type: Journal Article
• Authors: Fortini, Francesca; Vieceli Dalla Sega, Francesco; Caliceti, Cristiana; Lambertini, Elisabetta; Pannuti, Antonio; Peiffer, Daniel S.; Balla, Cristina; Rizzo, Paola
• Is Part Of: Journal of steroid biochemistry and molecular biology. Issue 189(2019)
• Page Start: 87
• Page End: 100
• Publication Date: 2019-05
• Subjects: Estrogen -- Endothelial dysfunction -- Notch -- Inflammation -- Hormone therapy -- Coronary heart disease; Steroid hormones -- Periodicals; Biochemistry -- Periodicals; Hormones -- Periodicals; Molecular Biology -- Periodicals; Hormones stéroïdes -- Périodiques; Steroid hormones; Periodicals; 572.579
• DOI: 10.1016/j.jsbmb.2019.02.008
• Languages: English
• ISSNs: 0960-0760

Abstract

Highlights: Endothelial apoptosis is a risk factor for coronary heart disease. Estrogen, through ERβ, increases endothelial Notch1. Notch1 is necessary to reduce TNFα - induced endothelial apoptosis. Notch1 inhibition for cancer therapy could cause endothelium dysfunction. ERβ specific drugs may prevent endothelial dysfunction after menopause. Abstract: Estrogen regulates a plethora of biological processes, under physiological and pathological conditions, by affecting key pathways involved in the regulation of cell proliferation, fate, survival and metabolism. The Notch receptors are mediators of communication between adjacent cells and are key determinants of cell fate during development and in postnatal life. Crosstalk between estrogen and the Notch pathway intervenes in many processes underlying the development and maintenance of the cardiovascular system. The identification of molecular mechanisms underlying the interaction between these types of endocrine and juxtacrine signaling are leading to a deeper understanding of physiological conditions regulated by these steroid hormones and, potentially, to novel therapeutic approaches to prevent pathologies linked to reduced levels of estrogen, such as coronary heart disease, and cardiotoxicity caused by hormone therapy for estrogen-receptor-positive breast cancer.