自闭症谱系障碍中 TWEAK/Fn14 受体调节的假说。

Heena Khan, Vivek Rihal, Amarjot Kaur, Thakur Gurjeet Singh
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摘要

自闭症谱系障碍(ASD)是一种神经发育障碍,病因复杂多样,主要表现为社交、沟通和重复行为障碍。尽管自闭症的发病率在全球范围内不断上升,但目前还没有针对自闭症核心症状的药物治疗方法。自闭症谱系障碍的治疗涉及众多信号通路的相互作用,如 Wnt/beta-catenin 通路、益生菌和犬尿氨酸通路、PPAR 通路、PI3K-AKT-mTOR 通路、刺猬信号通路等。科学文献显示,TWEAK/Fn14 在自闭症谱系障碍中并没有被发现。在体外和体内,TWEAK 可控制多种细胞反应。最近的研究发现,TWEAK 和 Fn14 在中枢神经系统(CNS)中表达,并在血管周围内皮细胞、星形胶质细胞、神经元和小胶质细胞中上调,以应对包括脑缺血在内的各种刺激。这种上调会导致细胞死亡和血脑屏障(BBB)通透性增加。研究发现,三羧酸(ATA)是一种抑制 TWEAK/Fn14 信号传导的物质。同样,讨论还强调,所提出的 TWEAK/Fn14 信号分子通路可被视为治疗自闭症谱系障碍的一种方法。
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Proposed Hypothesis of TWEAK/Fn14 Receptor Modulation in Autism Spectrum Disorder.

Autism Spectrum Disorder (ASD) is a neurodevelopmental disorder with a complex, multiple etiology that is marked by impaired social interaction, communication, and repetitive behaviour. There is presently no pharmaceutical treatment for the core symptoms of ASD, even though the prevalence of ASD is increasing worldwide. Treatment of autism spectrum disorder involves the interaction of numerous signalling pathways, such as the Wnt/beta-catenin pathway, probiotics and kynurenine pathway, PPAR pathway, PI3K-AKT-mTOR pathway, Hedgehog signaling pathway, etc. The scientific literature has revealed TWEAK/Fn14 to not be explored in the autism spectrum disorder. In vitro and in vivo, TWEAK can control a wide range of cellular responses. Recent research has revealed that TWEAK and Fn14 are expressed in the Central Nervous System (CNS) and upregulated in perivascular endothelial cells, astrocytes, neurons, and microglia in response to various stimuli, including cerebral ischemia. This upregulation is followed by cell death and an increase in Blood-brain Barrier (BBB) permeability. The study has revealed that Aurintricarboxylic Acid (ATA) acts as an agent that suppresses TWEAK/Fn14 signaling. Similarly, from the discussion, it has been emphasized that the proposed molecular TWEAK/Fn14 signalling pathway can be considered as a therapeutic approach in the management of autism spectrum disorder.

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