帕金森病(PD),被称为最普遍的神经退行性疾病之一,是对老年人健康的严重威胁。目前的治疗已被证明可以缓解症状,发现新的小分子化合物被认为是一种有前途的策略。值得注意的是,自身溶酶体途径(ALP)的稳态与PD密切相关,自噬受损可能导致神经元死亡,从而加速PD的进展。因此,迄今为止,小分子化合物的药物靶向自噬已引起越来越多的关注.在这次审查中,我们专注于总结几个自噬相关的靶标,比如AMPK,mTORC1,ULK1,IMPase,LRRK2,beclin-1,TFEB,GCase,ERRα,C-Abelson,以及它们在PD模型中的相关小分子化合物,这将揭示在不久的将来利用更多潜在的靶向小分子药物追踪PD治疗的线索。
Parkinson\'s disease (PD), known as one of the most universal neurodegenerative diseases, is a serious threat to the health of the elderly. The current treatment has been demonstrated to relieve symptoms, and the discovery of new small-molecule compounds has been regarded as a promising strategy. Of note, the homeostasis of the autolysosome pathway (ALP) is closely associated with PD, and impaired autophagy may cause the death of neurons and thereby accelerating the progress of PD. Thus, pharmacological targeting autophagy with small-molecule compounds has been drawn a rising attention so far. In this review, we focus on summarizing several autophagy-associated targets, such as AMPK, mTORC1, ULK1, IMPase, LRRK2, beclin-1, TFEB, GCase, ERRα, C-Abelson, and as well as their relevant small-molecule compounds in PD models, which will shed light on a clue on exploiting more potential targeted small-molecule drugs tracking PD treatment in the near future.