الفهرس 
Skin AgingOnly 14 pages are availabe for public view
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Abstract
Skin aging is a multisystem degenerative process that involves the skin and skin support system. Aging caused by the genes we inherit and depending on the passage of time per se is called chronological or intrinsic aging. Intrinsic skin aging is characterized by atrophy of the skin with loss of elasticity and slowed metabolic activity. The signs of intrinsic aging are fine wrinkles, thin and transparent skin, loss of underlying fat, facial bone loss, dry skin. The other type of aging is known as extrinsic aging and is caused by environmental factors. Among harmful environmental factors that contribute to extrinsic aging, long term effects of repeated exposure to ultraviolet light are most significant and are referred to as photoaging.
Estrogen receptors are a group of proteins found inside cells. They are receptors that are activated by the hormone estrogen (17β-estradiol).
Two classes of estrogen receptor exist: ER, which is a member of the nuclear hormone family of intracellular receptors, and GPER, which is a member of the rhodopsin-like family of G protein-coupled receptors. This article refers to the former (ER). Once activated by estrogen, the ER is able to translocate into the nucleus and bind to DNA to regulate the activity of different genes.
It is well known that estrogen can prevent collagen loss, increase skin thickness, restore skin moisture, prevent hair loss and promote wound healing. Estrogen exerts its effects mainly via binding to estrogen receptors. In skin, a strong ER beta expression were detected in the epidermis, dermal fibroblasts, blood vessels, melanocytes) as well as hair follicles.. Estrogen can directly regulate fibroblasts function and increase the collagen content via promoting TGFB production. Moreover, estrogen can reverse epidermal atrophy via stimulating the proliferation and DNA synthesis of keratinocytes. It has been demonstrated that estrogen suppresses keratinocytes apoptosis and activate cell-cycle protein-cyclin D2, mainly via interacting with a G protein-coupled receptor for estrogen (GPR30),a cell-surface receptor, which further lead to cyclic adenosine monophosphate (cAMP)/protein kinase A (PKA)- signaling pathway activation.