内质网是真核细胞蛋白合成和折叠的主要细胞器,当内质网内蛋白合成或折叠负担增加,引起未折叠或错误折叠蛋白增多时,可激活内质网几条特定信号通路,启动未折叠蛋白反应,这对维持细胞稳态有重要意义。越来越多研究表明,多种炎性反应疾病与内质网应激有密切联系。一方面,内质网应激引起的未折叠蛋白反应可以诱发或者抑制炎症,另一方面,炎性反应也能影响蛋白折叠,从而促进或缓解内质网应激。2型糖尿病、肿瘤和动脉粥样硬化等多种重大疾病的病理机制都涉及内质网应激与炎性反应的相互作用,对该问题的深入研究不仅能加深人们对这些疾病发病机制的理解,也有助于相关药物的研发。
Endoplasmic reticulum(ER) is the primary organelle in which protein is synthesised and folded. Increasing protein synthesis beyond the capacity of ER will induce accumulation of unfolded/misfolded pro- teins and trigger the unfolded protein response(UPR) or ER stress. ER stress or UPR is not only critical for cell homeostasis, but also critical for inflammatory diseases.ERS and UPR can induce or inhibit inflammatory responses. Conversely, inflammatory responses can aggratate or alleviate ERS through affecting protein folding.The interaction between ERS and inflammatory responses is involved in pathomechanism of many diseases,including type 2 diabetes,cancer and atherosclerosis.The progress in this subject may result in approaches to understand the mechanism and to invent new medicine.