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Published on: August 13, 2019
Effect of dehydroepiandrosterone on atherosclerosis in postmenopausal women
Siwei Zhang1,2,3, Jing Zhou1,2,3, Lijuan Li1,2,3
1Laboratory for Reproductive Immunology, Hospital and Institute of Obstetrics and Gynecology, Shanghai Medical College, Fudan University, Shanghai, China.
Insights
Dehydroepiandrosterone (DHEA) combats atherosclerosis (AS) by improving lipid status, protecting endothelial cells, and inhibiting vascular smooth muscle cell proliferation, offering therapeutic value for cardiovascular disease (CVD) in postmenopausal women.
Area of Science:
- Endocrinology
- Cardiovascular Medicine
- Pathology
Background:
- Cardiovascular disease (CVD) is the leading cause of mortality in China, with atherosclerosis (AS) as a primary pathological driver.
- Dehydroepiandrosterone (DHEA), an abundant steroid hormone, serves as a precursor to sex hormones and exhibits therapeutic potential.
- Postmenopausal women exhibit increased susceptibility to AS and CVD due to decreased ovarian function.
Purpose of the Study:
- To analyze the mechanisms underlying postmenopausal women's increased susceptibility to atherosclerosis (AS).
- To review the therapeutic mechanisms by which Dehydroepiandrosterone (DHEA) combats AS in postmenopausal women.
- To highlight the potential of DHEA in preventing and treating AS and CVD in this demographic.
Main Methods:
- Review of existing literature on atherosclerosis (AS) pathogenesis in postmenopausal women.
- Analysis of Dehydroepiandrosterone's (DHEA) molecular and cellular mechanisms against AS.
- Examination of DHEA's effects on lipid profiles, endothelial cells (ECs), and vascular smooth muscle cells (VSMCs).
Main Results:
- Postmenopausal women experience dyslipidemia, increased vascular smooth muscle cell (VSMC) proliferation/migration, and heightened oxidative stress and inflammation in endothelial cells (ECs).
- DHEA effectively regulates blood lipid status, protects ECs from oxidative stress and inflammation, inhibits EC apoptosis, and promotes nitric oxide (NO) production.
- DHEA significantly inhibits VSMC proliferation and migration, key processes in AS development.
Conclusions:
- DHEA demonstrates significant therapeutic value in preventing and inhibiting the progression of atherosclerosis (AS) in postmenopausal women.
- DHEA's multifaceted actions on lipid metabolism, endothelial function, and vascular smooth muscle cells make it a promising agent against CVD.
- Targeting DHEA offers a strategy to mitigate the increased cardiovascular disease (CVD) risk associated with menopause.
Abstract:
In China, cardiovascular disease (CVD) has surpassed malignant tumours to become the disease with the highest mortality rate, and atherosclerosis (AS) is an important pathological cause of CVD. Dehydroepiandrosterone (DHEA) is the most abundant steroid hormone in circulating human blood and is a precursor of estrogen and androgen. DHEA is converted into a series of sex hormones in local peripheral tissues where its acts physiologically. DHEA also acts therapeutically, thereby avoiding the adverse systemic reactions to sex hormones. DHEA inhibits AS, thus inhibiting the development of CVD, and it improves the prognosis for CVD. The incidence of CVD in postmenopausal women is substantially higher than that in premenopausal women, and that incidence is believed to be related to a decrease in ovarian function. The current review analyzes the mechanisms of postmenopausal women's susceptibility to AS. They tend to have dyslipidemia, and their vascular smooth muscle cells (VSMCs) proliferate and migrate more. In addition, oxidative stress and the inflammatory response of endothelial cells (ECs) are more serious in postmenopausal women. This review also discusses how DHEA combats AS by countering these mechanisms, which include regulating the blood lipid status, protecting ECs (including coping with oxidative stress and inflammatory reactions of the vascular endothelium, inhibiting apoptosis of ECs, and inducing NO production) and inhibiting the proliferation and migration of VSMCs. As a result, DHEA has great value in preventing AS and inhibiting its progression in postmenopausal women.
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