Activation of hepatic USP5 as a novel strategy to ameliorate metabolic dysfunction-associated steatotic liver disease by deubiquitinating CPT-1A
本研究确定肝脏 USP5 是代谢功能障碍相关脂肪性肝病(MASLD)的关键治疗靶点,证明了 USP5 通过去除 K6 连接的泛素链来稳定脂肪酸氧化酶 CPT-1A,并且 USP5 激活剂木犀 cursorPos 能够通过恢复这一调节轴有效改善 MASLD 症状。