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胆脂瘤上皮细胞存在异常的高度增殖能力,胆脂瘤基质周围新生血管形成和微循环的重建为胆脂瘤上皮的异常增殖提供较丰富的血供和营养。胆脂瘤上皮由于受到所处微环境中的炎症因子、细胞因子的刺激,导致基质金属蛋白酶家族(MMPs)高表达并诱导新生血管形成。MMPs在血管生成作用中不只是起到降解细胞外基质(ECM)作用,它们还可以通过调整内皮细胞黏附、增殖、转移和生长或者直接通过释放基质中隐藏的血管生长因子促进血管生成。此外,ECM涉及组织稳态和肿瘤浸润及炎症等病理过程,MMPs和TIMPs是维持ECM稳态的重要因素,MMPs-TIMPs活力失衡可能对胆脂瘤增殖及骨质破坏吸收有重要影响。
Cholesteatoma epithelial cells have an abnormally high proliferative capacity, neovascularization around the matrix of cholesteatoma and microcirculation reconstruction provide abundant blood supply and nutrition for the abnormal proliferation of cholesteatoma epithelium. Cholesteatoma epithelium is stimulated by inflammatory factors and cytokines in the microenvironment, resulting in high expression of matrix metalloproteinases (MMPs) and induction of neovascularization. MMPs do more than just degrade the extracellular matrix (ECM) during angiogenesis, they can also promote angiogenesis by regulating endothelial cell adhesion, proliferation, metastasis and growth or directly by releasing hidden vascular growth factors in the matrix. In addition, ECM involves the pathological process of tissue homeostasis, tumor infiltration and inflammation. MMPs and TIMPs are important factors in maintaining ECM homeostasis. The imbalance of MMPs-TIMPs may play an important role in the proliferation and destruction of cholesteatoma.