神经营养因子作用于Trk受体酪氨酸激酶后能激活细胞内磷酸肌醇3-激酶、细胞外信号调节激酶等信号通路,促进神经元的存活和分化。开发非肽类小分子Trk激动剂以及神经营养因子模拟物,能够在激动Trk受体信号转导的同时避免神经营养因子的诸多缺点,为治疗神经系统疾病提供了新的治疗思路。 After acting on Trk receptor tyrosine kinase, neurotrophic factors can activate intracellular phosphoinositide 3-kinase and extracellular signal-regulated kinase and other signaling pathways to promote the survival and differentiation of neurons. The development of non-peptide small molecule Trk agonists and neurotrophic factor mimics can avoid many shortcomings of neurotrophic factors while stimulating Trk receptor signal transduction and provide a new therapeutic approach for the treatment of nervous system diseases.