Author/Authors :
Mennander, Ari Division of Cardiothoracic Surgery - Tampere University Heart Hospital and Tampere University - Tampere - Finland , Valtonen, Nitta-Nea Department of Pathology - Fimlab Laboratories and Tampere University - Tampere - Finland , Niinimäki, Eetu Department of Pathology - Fimlab Laboratories and Tampere University - Tampere - Finland , Kholová, Ivana Department of Pathology - Fimlab Laboratories and Tampere University - Tampere - Finland , Paavonen, Timo Department of Pathology - Fimlab Laboratories and Tampere University - Tampere - Finland
Abstract :
There is increasing awareness that the aortic valve may
be involved in the pathophysiology of the ascending aorta (1).
Age, sex, and osteoporosis may impact the physiopathology of
atherosclerosis and aortic valve stenosis (2-5), along with reninangiotensin activation, nitric oxide, and noradrenaline (4). Structurally, the aortic valve is directly connected to the media layer
of the ascending aorta, highlighting the important functional and
anatomical connection of the aortic valve, the aortic root, and
the ascending aorta (e.g., a severely stenotic aortic valve is often
found inside a stiff atherosclerotic aortic root) (1).
As steroid hormones, estrogens have gained abundant interest in terms of vascular pathology (2). There are 2 different estrogen receptors (ER), ER1 and ER2. In particular, ER2 modulates
the vasculature through inflammation, regulates smooth muscle
cells proliferation, the vascular tone, and neovascularization (6,
7), all of which play a role in inducing anti-atherosclerosis (6).
