LGR5型
大麻酚
干细胞
细胞生物学
转录组
化学
再生(生物学)
脂类学
癌症研究
丁酸盐
生物
生物化学
姜黄素
药理学
细胞生长
下调和上调
孤雌内酯
作者
Zebin Liao,Congshu Huang,Liangliang Zhang,Changkun Hu,Zekun Wu,Zhijie Bai,Gaofu Li,Lei Zhou,Hongtao Wang,Chaoji Huangfu,Zhexin Ni,Pan Shen,Wei Zhou,Yue Gao
标识
DOI:10.1038/s12276-026-01711-5
摘要
ISCs proliferation upon a lethal dose of IR. Using absolute quantitative lipidomics, we found that the dysregulation of fatty acids in crypts induced by IR was rescued by CBD, which was indispensable for ISCs regeneration. Integrative analysis of transcriptome and lipidomics unveiled the critical role of PPARα in regulating fatty acid β-oxidation (FAO) by transcriptionally upregulating Slc27a2 and Acox1. Further experiments showed that CBD could trigger the enrichment of Stat2 on the promoter region of Pparα, ultimately facilitating the FAO program and subsequent ISCs proliferation following IR exposure. In addition,THOC3 was identified as a direct target of CBD, which stabilized the THOC3 protein and substantially alleviated the IR-induced blockade of Stat2 mRNA nuclear export. This study reveals a connection between CBD-driven ISCs proliferation and the FAO program during IR damage, providing a promising avenue for IR-induced gastrointestinal syndrome treatment. The binding of CBD to THOC3 maintains its radiation stability, which then supports the nuclear export of Stat2 mRNA for the subsequent transactivation of Pparα. The upregulation of PPARα will ultimately stimulate the FAO program, thereby facilitating ISCs regeneration during IR exposure.
科研通智能强力驱动
Strongly Powered by AbleSci AI