SIRT1与子宫内膜异位症发病机制相关的研究进展

Research progress on the correlation between SIRT1 and the pathogenesis of endometriosis

摘要:

子宫内膜异位症（EMs）是一种妇科常见的良性疾病，其病因复杂多样且因异位内膜病灶具有增殖、黏附、侵袭、迁移等恶性肿瘤的特征，严重影响妇女患者的身心健康。EMs具体发病机制尚不明确，EMs的发病与炎症、氧化应激、血管生成等病理学发展过程密切相关。沉默信息调节因子1（SIRT1）作为一种组蛋白脱乙酰酶，可能通过调节组蛋白和关键转录因子的乙酰化过程介导免疫炎症反应、血管生成、氧化应激、细胞凋亡及自噬、上皮-间质转化等过程参与EMs发生、发展。近年来研究发现，一些天然产物可能通过靶向SIRT1及其相关途径来预防和治疗EMs，有可能成为临床中EMs的潜在治疗剂。该文综述SIRT1参与EMs发病潜在机制并讨论SIRT1作为EMs治疗靶点的潜力以及相关天然产物作为临床药物或膳食补充剂的有效性，以期为寻找EMs新的治疗靶点和开发具有良好药效学特性的抗EMs药物提供一些新的思路和方向。

Abstract:

Endometriosis (EMs) is a common benign gynecological disease, with a complex and diverse etiology. Ectopic endometrial lesions exhibit characteristics of malignant tumors, such as proliferation, adhesion, invasion, and migration, which seriously affect the physical and mental health of female patients. The specific pathogenesis of EMs is not yet clear, and previous studies have shown that the development of EMs is closely related to pathological processes including inflammation, oxidative stress, and angiogenesis. Silent information regulator 1 (SIRT1), as a histone deacetylase, may mediate immune inflammatory response, angiogenesis, oxidative stress, apoptosis, autophagy, epithelial-mesenchymal transition, and other processes by regulating the acetylation of histones and key transcription factors, and therefore play roles in the occurrence and development of EMs. In recent years, researches have found that some natural products may be able to prevent and treat EMs by targeting SIRT1 and its related pathways, and could be potential therapeutic agents for EMs in clinical practice. We summarize the underlying mechanisms by which SIRT1 is involved in the pathogenesis of EMs and discuss the potential of SIRT1 as a therapeutic target for EMs, as well as the effectiveness of related natural products as clinical drugs or dietary supplements, in order to provide new ideas and directions for identifying novel therapeutic targets for EMs and developing drugs with favorable pharmacodynamic properties against EMs.