引言
特发性肺纤维化(Idiopathic Pulmonary Fibrosis,IPF)是一种进展迅速且致命的纤维化疾病,患者诊断后的中位生存时间仅为2-4年【1,2】。现有的两个药物—吡非尼酮和尼达尼布,虽然能够减缓IPF疾病的进展,但并未显著改善患者的生存率。因此,IPF仍然是一个重大的健康挑战,迫切需要发现新的治疗靶点和开发新的更安全有效的治疗方法。
2024年8月2日,北京生命科学研究所/清华大学生物医学交叉研究院汤楠团队,与中日友好医院的代华平团队和普沐生物科技有限公司的研发团队合作,在Cell Stem Cell在线发表了题为Sustained amphiregulin expression in intermediate alveolar stem cells drives progressive fibrosis的研究论文。该研究揭示了损伤诱导的中间态肺泡干细胞及其表达的Amphiregulin(AREG)与特发性肺纤维化疾病的发生发展的密切相关,并通过中和抗体靶向AREG成功治疗动物模型的肺纤维化,证明了AREG是可用于治疗肺纤维化疾病的新靶点。这一发现不仅加深了对IPF病理机制的理解,还为开发疾病的治疗方法提供了新策略。


图1:中间态肺泡干细胞促纤维化发生的作用机制示意图(Credit: Cell Stem Cell)
综上,本研究基于进展性肺纤维化动物模型和临床转化医学研究系统性地揭示了中间态肺泡干细胞及其表达的AREG在肺纤维化发生和发展中的关键作用,并发现了其表达水平与IPF疾病严重程度成正相关(图1)。这一发现不仅解决了中间态的肺泡干细胞如何参与进行性肺纤维化的细胞和分子机制,加深了对IPF病理机制的理解,还为开发新的治疗方法提供了重要线索,让靶向肺泡干细胞中的AREG成为可能治疗IPF的一种新策略。此外,这一研究还为其他类型的纤维化疾病的研究提供了参考,提示靶向AREG在其他纤维化疾病中也具有潜在疗效。总之,本研究不仅对理解和治疗IPF具有重要意义,还可能对更广泛的纤维化疾病研究和治疗提供了新思路。参考文献
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排版|探索君
文章来源|“BioArt”
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