Abstract:
:Epidemiological, clinical and animal studies revealed that sex differences exist in the manifestation and outcome of cardiovascular disease (CVD). The underlying molecular mechanisms implicated in these sex differences are not fully understood. The reasons for sex differences in CVD are definitely multifactorial, but major evidence points to the contribution of sex steroid hormone, 17β-estradiol (E2), and its receptors, estrogen receptor alpha (ERα) and estrogen receptor beta (ERβ). In this review, we summarize past and present studies that implicate E2 and ER as important determinants of sexual dimorphism in the physiology and pathophysiology of the heart. In particular, we give an overview of studies aimed to reveal the role of E2 and ER in the physiology of the observed sex differences in CVD using ER knock-out mice. Finally, we discuss recent findings from novel transgenic mouse models, which have provided new information on the sexual dimorphic roles of ER specifically in cardiomyocytes under pathological conditions.
journal_name
Pharmacol Resjournal_title
Pharmacological researchauthors
Dworatzek E,Mahmoodzadeh Sdoi
10.1016/j.phrs.2017.01.019subject
Has Abstractpub_date
2017-05-01 00:00:00pages
27-35eissn
1043-6618issn
1096-1186pii
S1043-6618(16)30874-Xjournal_volume
119pub_type
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