Mechanisms of angioregression of the corpus luteum.

Mechanisms of angioregression of the corpus luteum.
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DOI:
10.3389/fphys.2023.1254943
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发表时间:
2023
影响因子:
4
通讯作者:
--
中科院分区:
医学2区
文献类型:
--
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黄体是一个短暂的卵巢内分泌腺,产生孕酮,是建立和维持妊娠所必需的。这个腺体的形成和功能涉及血管生成,建立组织具有强大的血液流动和巨大的微血管系统,这是支持孕激素产生所必需的。黄体内的每个类固醇生成细胞都与毛细血管直接接触,血管生成的中断会损害黄体的发育和功能。在生殖周期结束时,黄体停止孕酮的产生,并经历快速的结构退化为无功能的白念珠菌,这一过程由黄体素前列腺素F2α(PGF2α)启动和加剧。结构退化伴随着黄体微血管的完全退化,其中内皮细胞死亡并脱落到毛细血管和淋巴管中。在黄体退化期间,一氧化氮的变化会短暂增加血流量,随后会减少血流量和孕激素分泌。早期黄体退化的特点是细胞因子和趋化因子的产生增加以及免疫细胞的涌入。微血管内皮细胞在黄体溶解过程中对释放的因子非常敏感,包括血栓反应蛋白、内皮素以及肿瘤坏死因子α和转化生长因子β1等细胞因子。尽管PgF2α被认为是一种血管收缩因子,但内皮细胞不表达PgF2α受体,因此认为在黄体溶解过程中发生的血管退行性变是由PgF2α信号通路下游的因素介导的。然而,黄体血管退行性变的确切机制仍不清楚。本文综述了黄体血管退行性变的研究现状,以及黄体溶解过程中释放的血管活性因子对黄体血管和微血管内皮细胞的作用。
The corpus luteum is a transient ovarian endocrine gland that produces the progesterone necessary for the establishment and maintenance of pregnancy. The formation and function of this gland involves angiogenesis, establishing the tissue with a robust blood flow and vast microvasculature required to support production of progesterone. Every steroidogenic cell within the corpus luteum is in direct contact with a capillary, and disruption of angiogenesis impairs luteal development and function. At the end of a reproductive cycle, the corpus luteum ceases progesterone production and undergoes rapid structural regression into a nonfunctional corpus albicans in a process initiated and exacerbated by the luteolysin prostaglandin F2α (PGF2α). Structural regression is accompanied by complete regression of the luteal microvasculature in which endothelial cells die and are sloughed off into capillaries and lymphatic vessels. During luteal regression, changes in nitric oxide transiently increase blood flow, followed by a reduction in blood flow and progesterone secretion. Early luteal regression is marked by an increased production of cytokines and chemokines and influx of immune cells. Microvascular endothelial cells are sensitive to released factors during luteolysis, including thrombospondin, endothelin, and cytokines like tumor necrosis factor alpha (TNF) and transforming growth factor β 1 (TGFB1). Although PGF2α is known to be a vasoconstrictor, endothelial cells do not express receptors for PGF2α, therefore it is believed that the angioregression occurring during luteolysis is mediated by factors downstream of PGF2α signaling. Yet, the exact mechanisms responsible for angioregression in the corpus luteum remain unknown. This review describes the current knowledge on angioregression of the corpus luteum and the roles of vasoactive factors released during luteolysis on luteal vasculature and endothelial cells of the microvasculature.
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