Previously thought of as a nonselective digestion process, autophagy is now known to specifically degrade aggregated proteins and damaged cellular organelles through the action of autophagy receptors, which provides cellular quality control and maintains homeostasis. Autophagy receptors recognize and recruit specific cargoes to the autophagosome–lysosome pathway for degradation in ubiquitin-dependent and -independent manners, and their functions (in selective autophagy) are regulated by protein modifications, for example, phosphorylation and ubiquitination. Growing evidence has linked the genetic variants of autophagy receptors to neurodegenerative diseases and multiple experimental systems have validated their roles in modulating the disease process. Here, we review the recent advances in understanding the physiology and pathophysiology of autophagy receptors in selective autophagy, and discuss their potentials as therapeutic targets for neurodegenerative diseases.

自噬以前被认为是非选择性消化过程，现在已知通过自噬受体的作用特异性降解聚集的蛋白质和受损的细胞器，从而提供细胞质量控制并维持体内平衡。自噬受体识别并吞噬自噬体-溶酶体途径的特定货物，以泛素依赖性和非依赖性方式降解，它们的功能（在选择性自噬中）受蛋白质修饰的调节，例如磷酸化和泛素化。越来越多的证据将自噬受体的遗传变异与神经退行性疾病联系起来，并且多个实验系统已经验证了它们在调节疾病过程中的作用。这里，