内质网应激与巨噬细胞M1/M2极化的研究进展

Progress of endoplasmic reticulum stress and macrophage M1/M2 polarization

内质网应激(endoplasmic reticulum stress,ERS)与巨噬细胞M1/M2极化密切相关,在肿瘤疾病中ERS引起的未折叠蛋白反应能调控巨噬细胞向M1型方向极化而诱导炎症反应,在肺纤维化和动脉粥样硬化发病过程中能促进巨噬细胞向M2型方向极化而抑制炎症反应。因此,通过对二者关系的深入研究,可以更好地理解这些疾病的发病机制,也有助于研发新的治疗药物并提供新的治疗策略。

Endoplasmic reticulum stress （ERS） was closely related to the mechanism of macrophage M1/M2 polarization. The unfolded protein response （UPR） caused by ERS may be involved in the regulation of macrophage M1 polarization and induced inflammation. However, in the pulmonary fibrosis and atherosclerosisit, it promoted macrophage M2 polarization and elicited anti-inflammatory effects. The study of ERS would provide the evidences for discovering new targets of drugs and new therapeutic strategies for these diseases.