神经炎症
核受体
受体
孤儿受体
神经科学
医学
多发性硬化
生物
生物信息学
疾病
转录因子
免疫学
内科学
遗传学
基因
作者
Kiran T. Thakur,Heena Khan,Amarjot Kaur Grewal,Thakur Gurjeet Singh
标识
DOI:10.1016/j.intimp.2023.110845
摘要
Orphan receptors constitute a historically varied subsection of a superfamily of nuclear receptors. Nuclear receptors regulate gene expression in response to ligand signals and are particularly alluring therapeutic targets for chronic illnesses. Neuroinflammation and neurodegenerative diseases have been linked to these orphan nuclear receptors. Preclinical and clinical evidence suggests that orphan receptors could serve as future targets in neuroinflammation, such as Parkinson's disease (PD), Alzheimer's Disease (AD), Huntington's Disease (HD), Multiple Sclerosis (MS), and Cerebral Ischemia. Given the therapeutic relevance of certain orphan receptors in a variety of disorders, their potential in neuroinflammation remains unproven. There is substantial evidence that ligand-activated transcription factors have great promise for preventing neurodegenerative and neurological disorders, with certain orphan nuclear receptors i.e., PPARγ, NR4As, and orphan GPCRs holding particularly high potential. Based on previous findings, we attempted to determine the contribution of PPAR, NR4As, and orphan GPCRs-regulated neuroinflammation to the pathogenesis of these disorders and their potential to become novel therapeutic targets.
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