中文摘要：

细胞自噬（autophagy）是生物体广泛存在的细胞内自主降解过程。该过程通过自我吞噬细胞质成分和细胞器形成具有双层膜结构的自噬体， 与溶酶体融合实现细胞内物质的循环利用。细胞自噬在饥饿、 缺氧、 内质网胁迫、 病原入侵、 蛋白聚集等不良环境条件下实现自我挽救， 而细胞自噬的大量发生也是程序性细胞死亡（PCD）的启动和执行者之一。目前人们对自噬体分子组装和自噬发生的分子通路已有较深入的了解， 但仍然在很多重要问题上难以达成共识。本文结合我们的研究进展， 对昆虫细胞自噬的生物学意义和自噬体膜的来源问题进行综述和探讨。昆虫在营养相对匮乏的情况下发生低水平自噬（常态自噬）， 用于维持细胞内的新陈代谢和继续生存的需要。昆虫在摄食阶段受到过度饥饿的刺激， 在变态发育时期受到蜕皮激素（20E）的诱导， 幼虫组织细胞发生高水平自噬和凋亡（apoptosis）， 细胞表现为不可逆死亡， 过度饥饿导致幼虫发育迟缓或者死亡， 而20E导致幼虫蜕皮和幼虫组织退化或消亡。不同于酵母和高等动物细胞中的深入研究， 病原入侵是否和如何诱导昆虫细胞发生自噬， 目前尚缺乏足够的文献依据， 值得深入探讨。几乎所有的细胞器（内质网、 高尔基体、 线粒体）膜都可能是自噬体膜的来源， 这一问题在昆虫中也有待进一步诠释。

英文摘要：

Autophagy is a ubiquitous phenomenon of intracellular selfdegradation in living organisms. In order to recycle cellular substances during autophagy, cytoplasmic aggregates and organelles are engulfed into doublemembrane autophagosomes and finally delivered to lysosomes for degradation. Autophagy is initiated as an adaptive response for cell survival in unfavorable conditions, such as starvation, anoxia, endoplasmic reticulum stress, pathogen invasion and aggregation of dysfunctional proteins, while extensive autophagy can act as an initiator and executor of programmed cell death （PCD）. Although the molecular assembling of autophagosomes and induction of autophagic pathway have been extensively documented, it is hard to reach a consensus on some important issues. In this review, we summarized and discussed the biological significance of the occurrence of autophagy and the source of autophagosomal membrane in insects. Under the circumstance of mild starvation, low level of autophagy will be induced to activate basal metabolism and to maintain cell survival. Challenged with excessive starvation during the feeding phase or stimulated by ecdysone during metamorphic development, high level of autophagy and apoptosis are triggered in larval tissues which will undergo irreversible cell death. Starvation causes delays of larval growth and development and eventual lethality, while 20E result in molting and degradation of larval tissues. Different from the pioneering studies in yeast and vertebrates, there are still not enough documented evidences to address whether pathogenic invasion can stimulate low level of autophagy in insect cells. The issue that almost all of the organelles-derived membrane can serve to be the source of autophagosomal membranes remains to be further investigated.