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通过G蛋白偶联受体(GPCRs)对脑源性神经营养因子/酪氨酸激酶受体B(BDNF/TrkB)信号通路产生间接影响,这是治疗神经退行性疾病的一种新兴策略。

Indirect influence on the BDNF/TrkB receptor signaling pathway via GPCRs, an emerging strategy in the treatment of neurodegenerative disorders.

作者信息

Antonijevic Mirjana, Dallemagne Patrick, Rochais Christophe

机构信息

Université de Caen Normandie, Normandie Univ., CERMN, Caen, France.

出版信息

Med Res Rev. 2025 Jan;45(1):274-310. doi: 10.1002/med.22075. Epub 2024 Aug 24.

Abstract

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.

摘要

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。

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