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尘肺(pneumoconiosis)是目前危害我国职业人群最严重的一类职业病,是由含游离二氧化硅(SiO2)的粉尘进入肺内导致肺组织纤维化引起的,而肺泡巨噬细胞(alveolar macrophages,AMs)的凋亡是导致肺纤维化的病理基础[1]。目前比较公认的细胞凋亡通路有线粒体通路、内质网通路和细胞膜死亡受体通路,细胞膜死亡受体通路主要通过3条基本信号转导通路诱导细胞凋亡,即凋亡蛋白及配体(Fas/FasL)途径、肿瘤坏死因子及受体(TNF-α/TNFR)途径、肿瘤坏死因子相关凋亡诱导配体受体(TRAILR/TRAIL)途径。下面着重介绍这3
Pneumoconiosis is one of the most serious occupational diseases in our country. It is caused by dust containing free silica (SiO2) entering the lungs leading to pulmonary fibrosis. Alveolar macrophages (AMs) ) Apoptosis is the pathological basis of pulmonary fibrosis [1]. At present, the most commonly recognized apoptotic pathways are the mitochondrial pathway, the endoplasmic reticulum pathway and the cell death receptor pathway. The cell death receptor pathway mainly induces apoptosis through three basic signal transduction pathways, namely, the apoptosis protein and the ligand Fas / FasL pathway, tumor necrosis factor and receptor (TNF-α / TNFR) pathway, and tumor necrosis factor-related apoptosis-inducing ligand receptor (TRAILR / TRAIL) pathway. The following highlights these 3