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肺间质纤维化(PF)的病理生理过程及病因尚不十分清楚。已有研究表明多种细胞因子能够激活成纤维细胞(FB),使之转化为肌成纤维细胞(MB),MB合成释放大量细胞外基质(ECM)等成分,从而导致PF形成。目前对于PF中MB的来源主要有:肺部原有FB转化成为MB、肺泡上皮细胞(AEC)转化为MB、血液中的纤维细胞转化为肺MB等,其转化的主要调控因素包括:转化生长因子-β(TGF-β)、结缔组织生长因子(CTGF)、内皮素(ET)、白介素(IL)、磷酸酶基因(PTEN)、端粒酶等。MB可造成ECM的异常沉积、肺顺应性下降、分泌多种炎性介质加重肺泡上皮损伤。
Pulmonary interstitial fibrosis (PF) pathophysiology and etiology is not yet clear. It has been shown that a variety of cytokines can activate fibroblasts (FBs), convert them into myofibroblasts (MBs) and MB synthesize and release large amounts of extracellular matrix (ECM) and other components, resulting in the formation of PF. At present, the main sources of MB in PF are: the transformation of the original FB in the lung into MB, the conversion of the alveolar epithelial cells (AEC) to MB, the conversion of fibroblasts in the blood into pulmonary MB, etc. The main regulatory factors of transformation include: TGF-β, CTGF, ET, IL, PTEN, telomerase and so on. MB can cause abnormal deposition of ECM, decreased lung compliance, the secretion of a variety of inflammatory mediators aggravate alveolar epithelial damage.