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半胱天冬酶在子宫内膜异位症中的研究进展

Research Progress of Caspase in Endometriosis.

作者信息

Yang Yuan, Li Lei-Lei, Qi Yu-Xin, Liu Da-Jiang

机构信息

Department of Centre for Reproductive Medicine, The First Hospital of Lanzhou University, Lanzhou, 730000, China.

The First Clinical Medical College, Lanzhou University, Lanzhou, 730000, China.

出版信息

Reprod Sci. 2024 Jun;31(6):1496-1507. doi: 10.1007/s43032-023-01425-3. Epub 2024 Feb 12.

Abstract

Endometriosis, a common chronic gynecological disease, refers to the presence and proliferation of endometrial tissue in locations other than the uterine cavity. Approximately 6 to 10% of the population of women of childbearing age are known to have endometriosis; the most common clinical signs are pelvic pain and infertility. Although endometriosis is a benign disease, it exhibits some typical features of malignant tumors, such as proliferation, invasion, metastasis, and recurrence. Endometriosis is considered a chronic, inflammatory, and estrogen-dependent disease, and multiple factors contribute to its occurrence and development. In recent years, increasing attention has been given to the role of apoptosis in the pathogenesis of this disease. Some researchers believe that spontaneous apoptosis of the endometrium is critical in maintaining its normal structure and function, and abnormal apoptosis can promote the occurrence and development of endometriosis. Inflammation is another likely process in the pathogenesis of endometriosis. Inflammation mediates the adhesion, proliferation, differentiation, and invasion of ectopic lesions of endometriosis, primarily by regulating the function of immune cells and increasing the level of proinflammatory cytokines in body fluids. The ultimate initiators of apoptosis and inflammatory cell death (pyroptosis) are the caspase family proteases. In this article, we review the progress in recent years in caspase function as well as the possible role of these enzymes in the pathogenesis of endometriosis, indicating potential treatment strategies.

摘要

子宫内膜异位症是一种常见的慢性妇科疾病,指子宫内膜组织出现在子宫腔以外的部位并发生增殖。已知约6%至10%的育龄女性患有子宫内膜异位症;最常见的临床症状是盆腔疼痛和不孕。尽管子宫内膜异位症是一种良性疾病,但它表现出一些恶性肿瘤的典型特征,如增殖、侵袭、转移和复发。子宫内膜异位症被认为是一种慢性、炎症性和雌激素依赖性疾病,多种因素促成其发生和发展。近年来,细胞凋亡在该疾病发病机制中的作用受到越来越多的关注。一些研究人员认为,子宫内膜的自发凋亡对于维持其正常结构和功能至关重要,而异常凋亡会促进子宫内膜异位症的发生和发展。炎症是子宫内膜异位症发病机制中的另一个可能过程。炎症主要通过调节免疫细胞的功能和增加体液中促炎细胞因子的水平,介导子宫内膜异位症异位病灶的黏附、增殖、分化和侵袭。细胞凋亡和炎性细胞死亡(焦亡)的最终启动者是半胱天冬酶家族蛋白酶。在本文中,我们综述了近年来半胱天冬酶功能的研究进展以及这些酶在子宫内膜异位症发病机制中的可能作用,指出潜在的治疗策略。

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