抑制HDAC11会触发双模热生成通路,以规避脂肪细胞对catecholamine的抗性

Emma L Robinson1,2, Rushita A Bagchi1,2, Jennifer L Major1,2

  • 1Department of Medicine, Division of Cardiology.

概括

在脂肪细胞中抑制基因组脱乙酶11 (HDAC11) 会促进脱蛋白1 (UCP1) 进行热生成. 这种方法即使在β-上腺素受体 (β-AR) 信号被阻断时也起作用,提供了一种新的治疗策略.

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