Antonijevic Mirjana, Dallemagne Patrick, Rochais Christophe
Université de Caen Normandie, Normandie Univ., CERMN, Caen, France.
Med Res Rev. 2025 Jan;45(1):274-310. doi: 10.1002/med.22075. Epub 2024 Aug 24.
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.
神经元的存活依赖于神经营养因子及其受体。神经营养因子受体有两种类型:肿瘤坏死因子受体(TNFR)家族的一种非酶促跨膜蛋白——p75受体,以及酪氨酸激酶受体(TrkR)A、B和C。脑源性神经营养因子(BDNF)或神经营养因子4/5(NT-4/5)激活TrkBR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G蛋白偶联受体(GPCR)和TrkR通过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,我们重点关注了不同GPCR及其配体在BDNF/TrkBR信号通路上的相互作用。