辐射旁效应已被证实存在与个体、组织和细胞间，其研究对于辐射防护的评估和精确放疗的应用有重要的意义。辐射旁效应目前被公认为通过两种机制介导的。其一是通过受辐照细胞的旁分泌作用产生的可溶性细胞因子在细胞间传播，其间涉及胞内激酶信号转导通路或者核内基因的表达调控，这一机制目前已有了比较系统的认识；另一机制则是通过细胞间缝隙连接（GJIC）介导的，而对于此过程的分子机制很少有研究涉及。细胞自噬系统是细胞内应急外界刺激的重要机关，并通过调节蛋白质量的动态平衡维持其生理功能。研究证实细胞在辐射刺激下能诱导细胞自噬系统的激活，参与组成细胞间通讯缝隙连接（GJIC）的关键组成分子connexin43自身也是细胞自噬系统的底物。因此，从细胞自噬系统的角度探讨对辐射诱导的旁效应的调控将有助于我们理解非靶效应产生的过程和机制，为调控靶和非靶效应在放射治疗中的作用打下基础。

Radiation-induced bystander effects (RIBEs) have been proved to exist among organs, tissues and cells, which have a significant role in evaluation of the radioprotection and radiotherapy. It's known now that RIBEs were mediated through two main ways. The first is that soluble factors secreted from the radiated cells diffuse in the cells, which involves the transduction of cellular kinase signaling and regulation on the expression of nuclear genes. This mechanism have been systematically studied. The second way is related with Gap junctional intercellular communication (GJIC), which the underlying mechanism was little studied. Autophagy system is a pivotal machinery in the cell that response to outer stress factors, which maintains the physiological function through regulating the dynamic balance of cellular proteins. It's reported that autophagy system was activated under the radiation stimulation. Moreover, the key molecule connexin43 involved in GJIC was a substrate of autophagy. As a result, it's important to further elucidate the process and mechanism of non-targetd effects by studying the regulation of RIBEs from the angle of autophagy system.