细胞自噬在神经病理性疼痛中的分子机制

Molecular mechanism of autophagy in neuropathic pain

神经病理性疼痛是由躯体感觉神经系统的损伤或疾病而直接造成的疼痛,涉及多种细胞、分子和通路。自噬参与神经病理性疼痛的生理病理过程,可能与炎症因子,氧化应激等机制有关。研究发现,mTOR、TLR、P62、Wnt、JNK、HIF等均参与神经病理性疼痛的自噬过程。在表观遗传学上,miRNA-195的可使外周神经损伤所致的自噬受到抑制,进而加剧神经病理性疼痛。神经病理性疼痛与自噬有关的各条通路又错综复杂,对神经病理性疼痛关于自噬的药物研发或治疗试验面临挑战。本文对细胞自噬与神经病理性疼痛的研究进展作一综述。

Neuropathic pain is a kind of pain directly caused by the injury or disease of somatosensory nervous system,involving a variety of cells,molecules and pathways.Autophagy is involved in the physiological and pathological process of neuropathic pain,which may be related to inflammatory factors,oxidative stress and other mechanisms.Studies have found that mTOR,TLR,P62,Wnt,JNK,HIF,etc.all participate in the autophagy process of neuropathic rational pain.In epigenetics,mirna-195 inhibits autophagy caused by peripheral nerve injury,which in turn intensifies neuropathic pain.The pathogenesis of autophagy in neuropathic pain is complicated,which challenges the research and development of drugs for autophagy in neuropathic pain.In this review,progress of the autophagy and neuropathic pain were summarized.