Update on the Role and Regulatory Mechanism of Extracellular Matrix in the Pathogenesis of Uterine Fibroids.

Update on the Role and Regulatory Mechanism of Extracellular Matrix in the Pathogenesis of Uterine Fibroids.
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更新细胞外基质在子宫肌瘤发病机理中的作用和调节机制。

DOI:
10.3390/ijms24065778
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发表时间:
2023-03-17
影响因子:
5.6
通讯作者:
--
中科院分区:
生物学2区
文献类型:
--
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子宫肌瘤(UFs),也称为平滑肌瘤,是子宫肌层的良性肿瘤,影响全球70%以上的女性,尤其是有色人种女性。虽然是良性的,但UFs与显著的发病率相关;它们是子宫切除术的主要指征,也是妇科和生殖功能障碍的主要来源,包括月经过多、盆腔疼痛、不孕症、复发性流产和早产。到目前为止,UFs发病机制的分子机制仍然非常有限。知识差距需要填补,以帮助制定新的策略,最终将促进治疗的发展和改善UF患者的结果。过度的ECM积累和异常重塑是纤维化疾病的关键,过度的ECM沉积是UFs的中心特征。本文从ECM产生的调控因子、ECM介导的信号转导以及针对ECM积累的药理药物等方面综述了近年来研究UFs的生物学功能和调控机制的进展。此外,我们通过讨论细胞外基质在UFs发病机制和应用中的调控和新兴作用的分子机制来提供当前的知识状态。全面而深入地了解细胞事件中ecm介导的改变和相互作用将有助于开发治疗这种常见肿瘤患者的新策略。
Uterine fibroids (UFs), also known as leiomyomas, are benign tumors of the myometrium affecting over 70% of women worldwide, particularly women of color. Although benign, UFs are associated with significant morbidity; they are the primary indication for hysterectomy and a major source of gynecologic and reproductive dysfunction, ranging from menorrhagia and pelvic pain to infertility, recurrent miscarriage, and preterm labor. So far, the molecular mechanisms underlying the pathogenesis of UFs are still quite limited. A knowledge gap needs to be filled to help develop novel strategies that will ultimately facilitate the development of therapies and improve UF patient outcomes. Excessive ECM accumulation and aberrant remodeling are crucial for fibrotic diseases and excessive ECM deposition is the central characteristics of UFs. This review summarizes the recent progress of ascertaining the biological functions and regulatory mechanisms in UFs, from the perspective of factors regulating ECM production, ECM-mediated signaling, and pharmacological drugs targeting ECM accumulation. In addition, we provide the current state of knowledge by discussing the molecular mechanisms underlying the regulation and emerging role of the extracellular matrix in the pathogenesis of UFs and in applications. Comprehensive and deeper insights into ECM-mediated alterations and interactions in cellular events will help develop novel strategies to treat patients with this common tumor.
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