TLR/mTOR 炎症信号通路:治疗精神分裂症的新见解。
TLR/mTOR inflammatory signaling pathway: novel insight for the treatment of schizophrenia.
发表日期:2023 Nov 13
作者:
Naser-Aldin Lashgari, Nazanin Momeni Roudsari, Hedieh Sadat Shamsnia, Maryam Shayan, Saeideh Momtaz, Amir Hossein Abdolghaffari
来源:
ANTIOXIDANTS & REDOX SIGNALING
摘要:
Toll 样受体 (TLR)/哺乳动物雷帕霉素靶点 (mTOR) 信号通路参与细胞内蛋白质合成调节,特别是介导神经元形态和促进突触可塑性的蛋白质合成。 TLR/mTOR 信号传导的活性被破坏,导致神经发育和突触可塑性缺陷,这是精神分裂症的主要症状。 TLR 受体激活 mTOR 信号通路并增加炎症细胞因子的升高。白细胞介素 (IL)-6 是最常见改变的细胞因子,而 IL-1、肿瘤坏死因子和干扰素 (IFN) 也会导致 SCZ。塞来昔布、阿司匹林、米诺环素和 omega-3 脂肪酸等抗炎和抗氧化药物已显示出对抗 SCZ 的功效。因此,可以建议抑制炎症过程来治疗 SCZ。因此,由于其炎症后果,mTOR/TLR 阻滞剂代表了 SCZ 的治疗方法。本工作的目的是寻找一种新型抗炎剂,可以阻断 mTOR/TLR 炎症信号通路,并为治疗神经炎症 SCZ 铺平道路。数据收集自 1998 年至 2022 年 10 月期间 Google Scholar、PubMed、Scopus 和 Cochrane 图书馆以英文发表的实验和临床研究。
The Toll-like receptor (TLR)/mammalian target of rapamycin (mTOR) signaling pathway is involved in the intracellular regulation of protein synthesis, specifically the ones that mediate neuronal morphology and facilitate synaptic plasticity. The activity of TLR/mTOR signaling has been disrupted, leading to neurodevelopment and deficient synaptic plasticity, which are the main symptoms of schizophrenia. The TLR receptor activates the mTOR signaling pathway and increases the elevation of inflammatory cytokines. Interleukin (IL)-6 is the most commonly altered cytokine, while IL-1, tumor necrosis factor, and interferon (IFN) also lead to SCZ. Anti-inflammatory and anti-oxidative agents such as celecoxib, aspirin, minocycline, and omega-3 fatty acids have shown efficiency against SCZ. As a result, inhibition of the inflammatory process could be suggested for the treatment of SCZ. So mTOR/TLR blockers represent the treatment of SCZ due to their inflammatory consequences. The objective of the present work was to find a novel anti-inflammatory agent that may block the mTOR/TLR inflammatory signaling pathways and might pave the way for the treatment of neuroinflammatory SCZ. Data were collected from experimental and clinical studies published in English between 1998 and October 2022 from Google Scholar, PubMed, Scopus, and the Cochrane library.