神经炎症
CD44细胞
疾病
神经退行性变
受体
炎症
生物
神经科学
医学
阿尔茨海默病
细胞生物学
生物信息学
小胶质细胞
退行性疾病
信号转导
神经保护
帕金森病
肌萎缩侧索硬化
作者
Meichen Zhang,Yongqi Lin,Huanhuan Wei,Qianqian Ju,Tong Gao,Yiyin Zhang,Lihua Shen,Cheng Sun
标识
DOI:10.1080/14728222.2025.2563243
摘要
INTRODUCTION: With the increasing prevalence of aging populations, the incidence of neurodegenerative diseases continues to rise, posing a serious threat to human health and quality of life. Owing to the highly complex pathogenesis of these disorders, the identification of effective therapeutic targets remains a major challenge. CD44, a cell surface glycoprotein, plays a central role in regulating cell proliferation, survival, adhesion, and migration. Emerging evidence further indicates that CD44 contributes to NF-κB activation, thereby amplifying inflammatory responses. AREAS COVERED: Given its central role in neuroinflammation, CD44 has attracted increasing attention as a potential therapeutic target for neurodegenerative diseases. This review explores the involvement of CD44 in amyotrophic lateral sclerosis (ALS), Alzheimer's disease (AD), and Parkinson's disease (PD), with particular emphasis on its contributions to neuroinflammatory processes, neuronal survival, and pathological protein aggregation. EXPERT OPINION: Chronic low-grade neuroinflammation is a major driver of neurodegenerative diseases, including ALS, AD, and PD. Growing evidence implicates CD44 as a key contributor to disease pathogenesis, with several studies reporting significantly elevated CD44 expression in affected patients. These findings highlight the role of CD44 in disease progression and suggest that targeting CD44-mediated inflammation may offer a promising therapeutic strategy for neurodegenerative disorders.
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