自噬涉及细胞质物质的隔离和递送到溶酶体,蛋白质,脂质,细胞器被降解和回收。根据细胞质成分被吞噬的方式,自噬可分为巨自噬,微自噬,和伴侣介导的自噬。最近,许多研究发现自噬在神经系统疾病中起重要作用,包括老年痴呆症,帕金森病,亨廷顿病,神经元兴奋性毒性,和脑缺血。自噬通过降解错误折叠的蛋白质维持神经系统中的细胞稳态,消除受损的细胞器,以及细胞凋亡和炎症的调节。AMPK-mTOR,Beclin1,TP53,内质网应激,和其他信号通路参与自噬的调节,可作为神经系统疾病的潜在治疗靶点。这里,我们讨论角色,功能,神经疾病中自噬的信号通路,这将揭示神经系统疾病的致病机制,并为治疗提供新的靶点。
Autophagy involves the sequestration and delivery of cytoplasmic materials to lysosomes, where proteins, lipids, and organelles are degraded and recycled. According to the way the cytoplasmic components are engulfed, autophagy can be divided into macroautophagy, microautophagy, and chaperone-mediated autophagy. Recently, many studies have found that autophagy plays an important role in neurological diseases, including Alzheimer\'s disease, Parkinson\'s disease, Huntington\'s disease, neuronal excitotoxicity, and cerebral ischemia. Autophagy maintains cell homeostasis in the nervous system via degradation of misfolded proteins, elimination of damaged organelles, and regulation of apoptosis and inflammation. AMPK-mTOR, Beclin 1, TP53, endoplasmic reticulum stress, and other signal pathways are involved in the regulation of autophagy and can be used as potential therapeutic targets for neurological diseases. Here, we discuss the role, functions, and signal pathways of autophagy in neurological diseases, which will shed light on the pathogenic mechanisms of neurological diseases and suggest novel targets for therapies.