Mount Sinai医学院的研究团队发现，一种名为AHR（芳基烃受体）的蛋白质在神经系统中起到"制动器"的作用，限制了受伤神经的再生能力。1研究表明，通过阻断这种蛋白或用药物抑制其活性，受损的轴突纤维可以更成功地再生。1该研究成果已发表于《Nature》杂志2026年653卷8116期。1
由Mount Sinai医学院神经外科和神经科学教授Hongyan Zou领导的研究团队在小鼠模型中验证了这一机制。1在周围神经损伤和脊髓损伤的实验中，抑制AHR改善了运动和感觉的恢复。1研究进一步阐明了AHR的双重作用：该蛋白支持蛋白质质量控制，帮助神经元承受细胞压力，但同时限制了轴突重建所需的新蛋白生成。1多种AHR抑制剂已正在进行其他病症的临床试验。1
Researchers at Mount Sinai School of Medicine have identified a protein that acts as a brake on nerve regeneration, explaining why injured nerves have difficulty recovering. The team, led by neurosurgery and neuroscience professor Hongyan Zou, found that the aryl hydrocarbon receptor (AHR) protein limits the ability of damaged nerve fibers to rebuild themselves.1 The findings, published in Nature in volume 653, issue 8116 (DOI: 10.1038/s41586-026-10295-z), suggest a new therapeutic avenue for treating nerve injuries.1
The study reveals that while AHR supports protein quality control mechanisms that help neurons withstand cellular stress, this protective function simultaneously suppresses the production of new proteins needed for axon regeneration.1 When researchers blocked AHR or inhibited its activity with drugs, damaged axon fibers showed improved regeneration in laboratory models.1 In mice with peripheral nerve injuries and spinal cord damage, suppressing AHR enhanced both motor and sensory recovery.1
The discovery opens possibilities for developing new treatments, particularly since multiple AHR inhibitors are already undergoing clinical trials for other conditions.1
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