ESTRADIOL: MECHANISM OF CARDIORENAL PROTECTION
Journal
Research in Physical Education, Sport and Health
Date Issued
2017
Author(s)
Abstract
Premenopausal women have a decreased incidence of cardiovascular disease and a decreased rate of progression of renal disease. With the onset of menopause, however, decreased synthesis of 17β-estradiol (estradiol) is accompanied by an increased incidence of cardiovascular disorders and accelerated progression of renal diseases. The glomerulus and the vascular wall are not static, and components of these structures dynamically increase, decrease, or reorganize in response to
physiological and pathological stimuli. Although multiple cellular and biochemical processes are
involved in glomerular and vascular remodelling, glomerular mesangial cells (GMCs) in the kidney and smooth muscle cells (VSMC) and endothelial cells in the vasculature are the final common pathway for dynamic changes in glomerular and vascular wall structure. Estradiol may induce protective effects on the renal and cardiovascular system by altering VSMC, GMC, or endothelial cell biology so as to prevent glomerular and vascular remodelling. The purpose of this review is to provide an overview of the participating mechanisms in this regard, as well as the mechanism of estradiol signalling in cardiomyocytes, with an emphasis on mechanisms that might be important in cardioprotection.
physiological and pathological stimuli. Although multiple cellular and biochemical processes are
involved in glomerular and vascular remodelling, glomerular mesangial cells (GMCs) in the kidney and smooth muscle cells (VSMC) and endothelial cells in the vasculature are the final common pathway for dynamic changes in glomerular and vascular wall structure. Estradiol may induce protective effects on the renal and cardiovascular system by altering VSMC, GMC, or endothelial cell biology so as to prevent glomerular and vascular remodelling. The purpose of this review is to provide an overview of the participating mechanisms in this regard, as well as the mechanism of estradiol signalling in cardiomyocytes, with an emphasis on mechanisms that might be important in cardioprotection.
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