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多囊卵巢综合征——卵巢卵泡中凋亡机制的丧失?

Polysystic ovary syndrome--loss of the apoptotic mechanism in the ovarian follicles?

作者信息

Homburg R, Amsterdam A

机构信息

Department of Ob/Gyn, Rabin Medical Center, Hasharon Hospital, Petah Tikva, Israel.

出版信息

J Endocrinol Invest. 1998 Oct;21(9):552-7. doi: 10.1007/BF03350780.

Abstract

Polycystic ovary syndrome (PCOS) is the most prevalent female endocrinopathy and the largest single cause of anovulatory infertility. The PCOS is characterized by multiple small antral follicles arrested in their development but nonatretic and viable. The hyperexpression of some growth factors (e.g. EGF/TGF alpha) in PCOS, considered to be survival or antiapoptotic factors, led to the hypothesis of their involvement in the blocking of apoptosis and atresia leading to an accumulation of multiple small antral follicles. Diminished FSH stimulation and accumulation of androgens could explain the arrest of progress to the preovulatory stage. Further investigation of the pathogenesis of PCOS is needed on the modulation of tumour suppressor and apoptosis genes such as p53, BAX or the APO/FAS system and the over expression of survival genes such as BCL2.

摘要

多囊卵巢综合征(PCOS)是最常见的女性内分泌疾病,也是无排卵性不孕的最大单一病因。PCOS的特征是多个小窦卵泡发育停滞,但未闭锁且存活。PCOS中某些生长因子(如表皮生长因子/转化生长因子α)的过度表达被认为是存活或抗凋亡因子,这导致了一种假说,即它们参与阻止凋亡和闭锁,从而导致多个小窦卵泡的积聚。促卵泡生成素(FSH)刺激减少和雄激素积累可以解释卵泡发育停滞在前排卵阶段的原因。需要进一步研究PCOS的发病机制,包括对肿瘤抑制基因和凋亡基因(如p53、BAX或APO/FAS系统)的调节以及存活基因(如BCL2)的过表达。

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