Department of Gynecology and Obstetrics, Johns Hopkins University, Baltimore, MD, USA.
Department of Obstetrics and Gynecology, Kuwait University, Kuwait City, Kuwait.
Biol Reprod. 2021 Jul 2;105(1):7-31. doi: 10.1093/biolre/ioab054.
Emerging evidence supports the notion that inflammation fosters the development of common benign gynecologic disorders, including uterine leiomyoma, endometriosis, and adenomyosis. Numerous cytokines, chemokines, and growth and transcription factors have indisputable roles in the establishment and maintenance of benign gynecologic disorders by initiating complex cascades that promote proliferation, angiogenesis, and lesion progression. The interaction between inflammation and benign gynecologic disorders is orchestrated by a plethora of factors, including sex steroids, genetics, epigenetics, extracellular matrix, stem cells, cardiometabolic risk factors, diet, vitamin D, and the immune system. The role of inflammation in these disorders is not limited to local pathobiology but also extends to involve clinical sequelae that range from those confined to the reproductive tract, such as infertility and gynecologic malignancies, to systemic complications such as cardiovascular disease. Enhanced understanding of the intricate mechanisms of this association will introduce us to unvisited pathophysiological perspectives and guide future diagnostic and therapeutic implications aimed at reducing the burden of these disorders. Utilization of inflammatory markers, microRNA, and molecular imaging as diagnostic adjuncts may be valuable, noninvasive techniques for prompt detection of benign gynecologic disorders. Further, use of novel as well as previously established therapeutics, such as immunomodulators, hormonal treatments, cardiometabolic medications, and cyclooxygenase-2 and NF-κB inhibitors, can target inflammatory pathways involved in their pathogenesis. In this comprehensive review, we aim to dissect the existing literature on the role of inflammation in benign gynecologic disorders, including the proposed underlying mechanisms and complex interactions, its contribution to clinical sequelae, and the clinical implications this role entails.
越来越多的证据支持这样一种观点，即炎症促进了常见良性妇科疾病的发展，包括子宫肌瘤、子宫内膜异位症和子宫腺肌病。许多细胞因子、趋化因子和生长及转录因子通过启动促进增殖、血管生成和病变进展的复杂级联反应，在良性妇科疾病的确立和维持中发挥着不可否认的作用。炎症与良性妇科疾病之间的相互作用是由大量因素协调的，包括性激素、遗传、表观遗传、细胞外基质、干细胞、心脏代谢危险因素、饮食、维生素 D 和免疫系统。炎症在这些疾病中的作用不仅限于局部病理生物学，还涉及从局限于生殖道的临床后果，如不孕和妇科恶性肿瘤，到心血管疾病等系统性并发症。增强对这种关联的复杂机制的理解，将使我们了解到未被探索的病理生理学观点，并指导未来旨在减轻这些疾病负担的诊断和治疗意义。炎症标志物、microRNA 和分子成像作为诊断辅助手段的应用可能是一种有价值的、非侵入性的技术，可用于快速检测良性妇科疾病。此外，新型和以前建立的治疗方法，如免疫调节剂、激素治疗、心脏代谢药物以及环氧化酶-2 和 NF-κB 抑制剂的应用，可以靶向参与其发病机制的炎症途径。在这篇全面的综述中，我们旨在剖析炎症在良性妇科疾病中的作用的现有文献，包括提出的潜在机制和复杂相互作用、其对临床后果的贡献以及该作用所带来的临床意义。
