斯坦福大学研究人员发现了一种通过阻断15-PGDH蛋白来促进软骨再生的方法，该蛋白水平随年龄增长约翻倍1。这一发现为关节炎治疗带来新的可能性1。
在动物实验中，该方法取得了显著成果1。接受15-PGDH抑制剂治疗的老年小鼠膝关节软骨变厚且功能改善1。在受到ACL样损伤后每周两次接受该抑制剂治疗四周的小鼠中，骨关节炎发展的可能性显著降低1，而未进行治疗的对照小鼠在同样时间内发展出了骨关节炎1。此外，从膝关节置换患者采集的人类软骨样本在接受相同抑制剂治疗后开始产生新的、功能性的关节软骨1。
这项研究具有重要的临床意义1。美国约五分之一的成年人患有骨关节炎，每年直接医疗成本约650亿美元1。一种15-PGDH抑制剂已在针对肌肉衰弱的临床试验中显示安全性和活性1。斯坦福大学教授Helen Blau表示："这是一种再生成人组织的新方法，对治疗因衰老或损伤引起的关节炎具有重要的临床前景"1。研究论文已发表于《科学》杂志2026年391卷第6789期1。
Researchers at Stanford University have identified a strategy to regenerate cartilage by blocking a protein that accumulates with age, potentially offering an alternative to joint replacement surgery.1 The protein 15-PGDH increases approximately twofold as people age, and inhibiting it appears to reverse cartilage loss and halt arthritis progression.1
In preclinical studies, aged mice treated with a 15-PGDH inhibitor showed thickened knee joint cartilage with improved function.1 When mice with ACL-like injuries received the inhibitor twice weekly for four weeks, they demonstrated significantly reduced likelihood of developing osteoarthritis, whereas untreated control mice developed the condition within the same timeframe.1 Human cartilage samples obtained from knee replacement patients similarly began generating new, functional joint cartilage when exposed to the same inhibitor.1
The findings carry substantial clinical implications given the prevalence of arthritis in the United States, where approximately one-fifth of adults have osteoarthritis, incurring roughly $65 billion in direct medical costs annually.1 A 15-PGDH inhibitor has already demonstrated safety and activity in clinical trials for muscle wasting, suggesting a potential pathway toward human application.1 Helen Blau, a lead researcher on the project, stated: "This is a new way to regenerate adult tissue with important clinical promise for treating arthritis caused by aging or injury."1 The research was published in Science in October 2026, Volume 391, Issue 6789, with DOI: 10.1126/science.adx6649.1
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