Review Article

肺癌和肺纤维化在癌症治疗中:细胞和分子机制研究进展

卷 23, 期 16, 2022

发表于: 04 October, 2022

页: [1505 - 1525] 页: 21

弟呕挨: 10.2174/1389450123666220907144131

价格: $65

摘要

肺纤维化和肺炎是癌症治疗后肺组织最重要的副作用。一些药物如博来霉素的放化疗可诱发肺炎和纤维化。与化疗和放疗相比,靶向治疗和免疫治疗也可能诱发肺炎和肺纤维化,但程度较小。免疫治疗活化淋巴细胞或化学/放疗后炎症细胞(如巨噬细胞、淋巴细胞、中性粒细胞和肥大细胞)浸润可诱发肺炎。此外,巨噬细胞向M2细胞的极化和抗炎细胞因子的释放刺激肺纤维化。肺纤维化和肺炎也可能因一些其他变化而增强,例如上皮间质转化 (EMT)、氧化应激、还原/氧化 (氧化还原) 反应、肾素-血管紧张素系统以及一些炎症介质的上调,例如NF-κB、炎症小体、环氧合酶-2 (COX-2) 和诱导性一氧化氮合酶 (iNOS)。肺血管系统的损伤和缺氧的诱导也会在化疗/放疗后诱发肺损伤。在本综述中,我们解释了癌症治疗后诱发肺炎和肺纤维化的各种机制。此外,还将讨论减轻肺纤维化和肺炎的目标和有希望的药物

关键词: 化学疗法,放射疗法,肺,纤维化,肺炎,上皮间质转化

图形摘要
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