肌萎缩侧索硬化症(ALS)是一种主要影响运动神经元的进行性神经退行性疾病,导致残疾和神经元死亡,和ATP结合盒(ABC)转运蛋白由于它们在药物外排和各种细胞途径的调节中的作用而导致ALS的发病机理。在这篇文章中,我们广泛研究了将ALS转运蛋白与ALS发病机理联系起来的各种分子和机制途径;这涉及炎症途径,如丝裂原激活蛋白激酶(MAPK),磷脂酰肌醇-3-激酶/蛋白激酶B(PI3K/Akt),Toll样受体(TLR),糖原合成酶激酶3β(GSK-3β),核因子κB(NF-κB),和环氧合酶(COX)。氧化途径,如星形胶质细胞,谷氨酸,核因子(红系衍生的2)样2(Nrf2),Sirtuin1(SIRT-1),叉头盒蛋白O(FOXO),细胞外信号调节激酶(ERK)。此外,我们深入研究了自噬途径的作用,如TARDNA结合蛋白43(TDP-43),AMP激活蛋白激酶(AMPK),哺乳动物雷帕霉素靶蛋白(mTOR),最后,凋亡途径。此外,通过理解这些复杂的相互作用,我们的目标是开发针对ABC转运蛋白的新型治疗策略,改善药物输送,并最终为治疗ALS提供了一个有希望的途径。
Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative primarily affecting motor neurons, leading to disability and neuronal death, and ATP-Binding Cassette (ABC) transporter due to their role in drug efflux and modulation of various cellular pathways contributes to the pathogenesis of ALS. In this article, we extensively investigated various molecular and mechanistic pathways linking ALS transporter to the pathogenesis of ALS; this involves inflammatory pathways such as Mitogen-Activated Protein Kinase (MAPK), Phosphatidylinositol-3-Kinase/Protein Kinase B (PI3K/Akt), Toll-Like Receptor (TLR), Glycogen Synthase Kinase 3β (GSK-3β), Nuclear Factor Kappa-B (NF-κB), and Cyclooxygenase (COX). Oxidative pathways such as Astrocytes, Glutamate, Nuclear factor (erythroid-derived 2)-like 2 (Nrf2), Sirtuin 1 (SIRT-1), Forkhead box protein O (FOXO), Extracellular signal-regulated kinase (ERK). Additionally, we delve into the role of autophagic pathways like TAR DNA-binding protein 43 (TDP-43), AMP-activated protein kinase (AMPK), mammalian target of rapamycin (mTOR), and lastly, the apoptotic pathways. Furthermore, by understanding these intricate interactions, we aim to develop novel therapeutic strategies targeting ABC transporters, improving drug delivery, and ultimately offering a promising avenue for treating ALS.