Dong Da-Long, Jin Guang-Zhen
Institute of Tissue Regeneration Engineering (ITREN), Dankook University, Cheonan 31116, Republic of Korea.
Department of Nanobiomedical Science and BK21 PLUS NBM Global Research Center for Regenerative Medicine, Dankook University, Cheonan 31116, Republic of Korea.
Bioengineering (Basel). 2025 Jan 15;12(1):77. doi: 10.3390/bioengineering12010077.
Osteoarthritis (OA) is a common joint disease characterized by pain and functional impairment, which severely impacts the quality of life of middle-aged and elderly individuals. During normal bone development, chondrocyte hypertrophy is a natural physiological process. However, in the progression of OA, chondrocyte hypertrophy becomes one of its key pathological features. Although there is no definitive evidence to date confirming that chondrocyte hypertrophy is the direct cause of OA, substantial experimental data indicate that it plays an important role in the disease's pathogenesis. In this review, we first explore the mechanisms underlying chondrocyte hypertrophy in OA and offer new insights. We then propose strategies for inhibiting chondrocyte hypertrophy from the perspectives of targeting signaling pathways and tissue engineering, ultimately envisioning the future prospects of OA treatment.
骨关节炎(OA)是一种常见的关节疾病,其特征为疼痛和功能障碍,严重影响中老年人的生活质量。在正常骨骼发育过程中,软骨细胞肥大是一个自然的生理过程。然而,在OA的进展过程中,软骨细胞肥大成为其关键的病理特征之一。尽管迄今为止尚无确凿证据证实软骨细胞肥大是OA的直接病因,但大量实验数据表明它在该疾病的发病机制中起重要作用。在本综述中,我们首先探讨OA中软骨细胞肥大的潜在机制并提供新的见解。然后我们从靶向信号通路和组织工程的角度提出抑制软骨细胞肥大的策略,最终展望OA治疗的未来前景。