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Updated: Feb 5, 2026

Isolation of Murine Coronary Vascular Smooth Muscle Cells
Published on: May 30, 2016
Estrogen in vascular smooth muscle cells: A friend or a foe?
Hassan Dehaini1, Manal Fardoun2, Haissam Abou-Saleh3
1Department of Pharmacology and Toxicology, American University of Beirut, Beirut, Lebanon.
Insights
Estrogen
Area of Science:
- Cardiovascular biology
- Endocrinology
- Cellular physiology
Background:
- Cardiovascular disease (CVD) is a leading global cause of mortality.
- Estrogen's role in cardiovascular health is debated, with conflicting evidence from clinical studies.
- Hormone replacement therapy (HRT) has not definitively proven cardiovascular benefits.
Purpose of the Study:
- To review the complex effects of estrogen on vascular smooth muscle cells.
- To explore the 'timing and opportunity' theory explaining estrogen's paradoxical cardiovascular effects.
- To discuss signaling pathways and molecular players involved in estrogen's vascular actions.
Main Methods:
- Review of in vitro, in vivo, and observational studies on estrogen and cardiovascular disease.
- Critical analysis of cellular mechanisms, focusing on vascular smooth muscle cell proliferation and migration.
- Discussion of key signaling pathways and molecular mediators.
Main Results:
- Estrogen exhibits both potentially protective and pathological effects on vascular smooth muscle cells.
- The 'timing and opportunity' theory suggests age-dependent estrogen effects are crucial.
- Conflicting outcomes are linked to specific cellular processes like proliferation and migration.
Conclusions:
- Estrogen's cardiovascular impact is complex and context-dependent, particularly regarding cell function.
- The age at which estrogen is administered significantly influences its effects.
- Further research into molecular mechanisms is needed to reconcile paradoxical findings.
Abstract:
Cardiovascular disease (CVD) continues to be the leading cause of death worldwide. The effect of estrogen on these diseases has been assessed in in vitro and in vivo models, as well as in observational studies. Collectively, these studies alluded to a cardiovasculo-protective effect of estrogen. However, comprehensive clinical investigation failed to produce concrete proof of a cardiovascular protective effect for hormone replacement therapy (HRT), let alone rule out potential harm. These seemingly paradoxical effects of estrogen were explained by the 'theory of timing and opportunity'. This theory states that the effect of estrogen, whether cardiovasculo-protective or pathological, significantly depends on the age of the individual when estrogen administration takes place. Here, we review the conflicting effects of estrogen on vascular smooth muscle cells, mainly proliferation and migration as two cellular capacities intimately related to physiology and pathophysiology of the cardiovascular system. Furthermore, we critically discuss the major parameters and signaling pathways that may account for the aforementioned paradoxical observations, as well as the key molecular players involved.
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