Cytosolic phospholipase A2 as a therapeutic target for degenerative joint diseases

软骨 骨关节炎 软骨细胞 衰老 变性(医学) 炎症 磷脂酶A2 调解人 生物 基质金属蛋白酶 医学 胞浆 退行性疾病 退行性疾病 发病机制 阿格里坎 病理 基因沉默 癌症研究 平衡 视网膜变性 磷脂酶 上睑下垂 细胞生物学
作者
Guiwu Huang,Chao He,Wenyu Fu,Jianlu Bi,Jianji Wang,Daniel H. Wiznia,Liu C
出处
期刊:Bone research [Springer Nature]
卷期号:13 (1): 86-86 被引量:3
标识
DOI:10.1038/s41413-025-00470-9
摘要

Osteoarthritis (OA) and intervertebral disc degeneration (IVDD) are degenerative musculoskeletal disorders characterized by degeneration of cartilaginous tissues and inflammation. While inflammation is implicated in the pathogenesis of OA and IVDD, and cytosolic phospholipase A2 (cPLA2) is a key mediator of inflammation, direct evidence linking cPLA2 to chondrocyte homeostasis and cartilage degeneration is lacking. This study aims to investigate the role of cPLA2 in chondrocytes and its contribution to the development of cartilage degenerative conditions such as OA and IVDD. Here, single-cell RNA sequencing was used to examine cPLA2 expression in chondrocytes. To explore its importance in chondrocytes and OA/IVDD, various cell-based assays and genetically modified mouse models with age-related and surgically induced OA/IVDD were employed. Furthermore, the therapeutic potential of fexofenadine, an over-the-counter drug recently identified as a cPLA2 inhibitor, was explored in these models. cPLA2 is predominantly expressed in prehypertrophic chondrocytes, characterized by elevated levels of cartilage degeneration markers and senescence-related genes. Genetic deletion and pharmacological inhibition of cPLA2 reduced inflammation induced catabolic activity and senescence in chondrocytes, as well as cartilage degeneration in various OA and IVDD models. This study identifies cPLA2 as a pivotal driver of cartilage degeneration and senescence in OA and IVDD, highlighting its potential as a dual-action therapeutic target that suppresses both inflammation and senescence to preserve cartilage integrity. These findings position cPLA2 as a promising candidate for developing disease-modifying therapies for cartilage degenerative conditions such as OA and IVDD.
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