The relevance of estrogen/estrogen receptor system on the gender difference in cardiovascular risk

- Thrombosis is at the basis of major cardiovascular disorders.
- There is a gender disparity in thrombogenesis.
- Estrogen/estrogen receptors (ERs) influence platelet functions and thrombogenicity.
- ERβ appears as the predominant form of ER in platelets.
- Non-nuclear estrogen receptor can trigger prompt functional response in platelets.

It has been reported that the incidence of thrombotic events can display a gender disparity. In particular, a lower thrombotic risk has been described in female gender. The mechanisms underlying this disparity are still poorly understood. Of great interest is the hypothesis that hormones, estrogen in particular, could play a key role. In fact, the possibility that some hormonal factors could protect women from thrombotic events appears well documented in literature. For instance, several studies aimed at the analysis of the impact of estrogen and estrogen receptors in thrombogenesis claim for the implication of these hormones either in megakaryocyte differentiation or, more intriguingly, directly affecting platelet integrity and function. In consideration of the absence of the nucleus, platelet susceptibility appears quite striking and probably due to the non-nuclear estrogen receptor function. In this review we briefly summarize our knowledge as concerns the role of estrogen and estrogen receptors in determining megakaryocyte/platelet functions and thrombogenicity.

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