通过 GPCR 对 BDNF/TrkB 受体信号通路产生间接影响,这是一种治疗神经退行性疾病的新兴策略。
Indirect influence on the BDNF/TrkB receptor signaling pathway via GPCRs, an emerging strategy in the treatment of neurodegenerative disorders.
发表日期:2024 Aug 24
作者:
Mirjana Antonijevic, Patrick Dallemagne, Christophe Rochais
来源:
Alzheimers & Dementia
摘要:
神经元的存活取决于神经营养蛋白及其受体。神经营养蛋白受体有两种类型:肿瘤坏死因子受体 (TNFR) 家族的非酶跨膜蛋白 - p75 受体和酪氨酸激酶受体 (TrkR) A、B 和 C。衍生神经营养因子 (BDNF) 或神经营养蛋白 4/5 (NT-4/5) 可促进神经元存活、分化和突触功能。研究表明,在几种神经退行性疾病(阿尔茨海默病、帕金森病、亨廷顿病)的发病机制中,BDNF/TrkBR 信号通路受损。由于已知 GPCR 和 TrkR 通过彼此相互作用并产生交叉通讯来调节多种细胞功能,因此在本综述中我们重点关注不同 GPCR 及其配体在 BDNF/TrkBR 信号通路上的相互作用。© 2024 Wiley periodicals有限责任公司。
Neuronal survival depends on neurotrophins and their receptors. There are two types of neurotrophin receptors: a nonenzymatic, trans-membrane protein of the tumor necrosis factor receptor (TNFR) family-p75 receptor and the tyrosine kinase receptors (TrkR) A, B, and C. Activation of the TrkBR by brain-derived neurotrophic factor (BDNF) or neurotrophin 4/5 (NT-4/5) promotes neuronal survival, differentiation, and synaptic function. It is shown that in the pathogenesis of several neurodegenerative conditions (Alzheimer's disease, Parkinson's disease, Huntington's disease) the BDNF/TrkBR signaling pathway is impaired. Since it is known that GPCRs and TrkR are regulating several cell functions by interacting with each other and generating a cross-communication in this review we have focused on the interaction between different GPCRs and their ligands on BDNF/TrkBR signaling pathway.© 2024 Wiley Periodicals LLC.