Brizuela Leyre, Buchet Rene, Bougault Carole, Mebarek Saida
Institut de Chimie et Biochimie Moléculaires et Supramoléculaires, Université de Lyon, Université Lyon 1, UMR CNRS 5246, 69 622 Villeurbanne Cedex, France.
Int J Mol Sci. 2025 Mar 22;26(7):2896. doi: 10.3390/ijms26072896.
Links between cathepsin K and the pathophysiology of osteoarthritis (OA) can be established, not least because of the overabundance of cathepsin K in the serum of OA patients and the upregulation of cathepsin K in degraded cartilage in animal models of OA. Chondrocytes, chondroclasts, or osteoclasts contribute to the accumulated cathepsin K at the diseased osteochondral junction. After a general presentation of OA and cartilage physiology, as well as its degradation processes, we describe the function of cathepsin K and its effect on cartilage degradation via type II collagen cleavage. An overview of the most promising cathepsin K inhibitors is then presented, together with their in vitro effects. Although intensive research on cathepsin K inhibitors initially focused on bone resorption, there is growing interest in the potential of these drugs to prevent cartilage degradation. In this review, we summarize the pre-clinical and clinical trials that support the use of cathepsin K inhibitors in the treatment of OA. To date, no molecules of this type are commercially available, although a few have undergone clinical trials, but we believe that the development of cathepsin K inhibitors could broaden the therapeutic arsenal for the treatment of OA.
组织蛋白酶K与骨关节炎(OA)病理生理学之间的联系是可以确立的,这尤其是因为OA患者血清中组织蛋白酶K含量过高,以及在OA动物模型中,退化软骨中组织蛋白酶K上调。软骨细胞、破软骨细胞或破骨细胞导致患病骨软骨交界处组织蛋白酶K积累。在对OA和软骨生理学及其降解过程进行总体介绍之后,我们描述了组织蛋白酶K的功能及其通过裂解II型胶原对软骨降解的影响。随后概述了最有前景的组织蛋白酶K抑制剂及其体外作用。尽管最初对组织蛋白酶K抑制剂的深入研究集中在骨吸收方面,但人们对这些药物预防软骨降解的潜力越来越感兴趣。在这篇综述中,我们总结了支持使用组织蛋白酶K抑制剂治疗OA的临床前和临床试验。迄今为止,这类分子尚无商业产品,尽管有几种已进入临床试验阶段,但我们认为,组织蛋白酶K抑制剂的研发可能会拓宽OA的治疗手段。