BACKGROUND It is well established that tumors are dependent on angiogenesis for their growth and survival. Although uterine fibroids are known to be benign tumors with reduced vascularization, recent work demonstrates that the vasculature of fibroids is grossly and microscopically abnormal. Accumulating evidence suggests that angiogenic growth factor dysregulation may be implicated in these vascular and other features of fibroid pathophysiology. METHODS Literature searches were performed in PubMed and Google Scholar for articles with content related to angiogenic growth factors and myometrium/leiomyoma. The findings are hereby reviewed and discussed. RESULTS Multiple growth factors involved in angiogenesis are differentially expressed in leiomyoma compared with myometrium. These include epidermal growth factor (EGF), heparin-binding-EGF, vascular endothelial growth factor, basic fibroblast growth factor, platelet-derived growth factor, transforming growth factor-β and adrenomedullin. An important paradox is that although leiomyoma tissues are hypoxic, leiomyoma feature down-regulation of key molecular regulators of the hypoxia response. Furthermore, the hypoxic milieu of leiomyoma may contribute to fibroid development and growth. Notably, common treatments for fibroids such as GnRH agonists and uterine artery embolization (UAE) are shown to work at least partly via anti-angiogenic mechanisms. CONCLUSIONS Angiogenic growth factors play an important role in mechanisms of fibroid pathophysiology, including abnormal vasculature and fibroid growth and survival. Moreover, the fibroid's abnormal vasculature together with its aberrant hypoxic and angiogenic response may make it especially vulnerable to disruption of its vascular supply, a feature which could be exploited for treatment. Further experimental studies are required in order to gain a better understanding of the growth factors that are involved in normal and pathological myometrial angiogenesis, and to assess the potential of anti-angiogenic treatment strategies for uterine fibroids.

中文翻译：

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血管生成因子在肌瘤发病机制中的作用：对未来治疗的潜在影响。

背景众所周知，肿瘤的生长和存活依赖于血管生成。尽管已知子宫肌瘤是血管形成减少的良性肿瘤，但最近的研究表明，肌瘤的血管系统在肉眼和显微镜下是异常的。越来越多的证据表明，血管生成生长因子失调可能与肌瘤病理生理学的这些血管和其他特征有关。方法 在 PubMed 和 Google Scholar 中进行文献搜索，以查找与血管生成生长因子和子宫肌层/平滑肌瘤相关内容的文章。特此审查和讨论调查结果。结果 与子宫肌层相比，平滑肌瘤中涉及血管生成的多种生长因子差异表达。这些包括表皮生长因子 (EGF)、肝素结合 EGF、血管内皮生长因子、碱性成纤维细胞生长因子、血小板衍生生长因子、转化生长因子-β和肾上腺髓质素。一个重要的悖论是，尽管平滑肌瘤组织是缺氧的，但平滑肌瘤的特征是对缺氧反应的关键分子调节因子进行下调。此外，平滑肌瘤的缺氧环境可能有助于肌瘤的发育和生长。值得注意的是，肌瘤的常见治疗方法如 GnRH 激动剂和子宫动脉栓塞 (UAE) 至少部分通过抗血管生成机制起作用。结论血管生成生长因子在肌瘤病理生理机制中发挥重要作用，包括异常脉管系统和肌瘤生长和存活。此外，肌瘤' 异常的脉管系统及其异常的缺氧和血管生成反应可能使其特别容易受到其血管供应中断的影响，这一特征可用于治疗。需要进一步的实验研究，以便更好地了解参与正常和病理性子宫肌层血管生成的生长因子，并评估子宫肌瘤抗血管生成治疗策略的潜力。