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目的：探讨转录辅助因子受体相互作用蛋白140( re-ceptor interacting protein 140, RIP140)与过氧化物酶体增殖物受体γ共激活因子1α( peroxisome proliferator-activated re-ceptor gamma coactivator-1α, PGC-1α)在血管紧张素Ⅱ( an-giotensin Ⅱ, AngⅡ)调节心肌细胞能量代谢中的作用。方法借助腺病毒载体系统诱导RIP140和PGC-1α基因过表达；利用荧光检测系统测定乳鼠心肌细胞线粒体ATP的含量；实时荧光定量PCR和Western blot的方法检测RIP140和PGC-1α的表达情况。结果乳鼠心肌细胞给予100 nmol· L-1 Ang Ⅱ刺激36 h后,心肌细胞线粒体ATP的含量降低(P<0．01),同时伴随RIP140 mRNA与蛋白水平的升高,而PGC-1αmRNA与蛋白水平下调。 AngⅡ诱导的ATP含量减少在过表达 RIP140组中进一步下降,而在过表达 PGC-1α组中有所减轻。结论 Ang Ⅱ诱导的 ATP 含量减少与RIP140表达上调和PGC-1α表达下调有关。“,”Aim To investigate the role of transcrip-tional cofactors receptor interacting protein 140 ( RIP140 ) and peroxisome proliferator-activated recep-tor γ coactivator-1α ( PGC-1α) in the angiotensin Ⅱ( AngⅡ) mediated energy metabolism regulation in cardiomyocytes. Methods RIP140 or PGC-1α was overexpressed via adenovirus vector system. ATP con-tents were detected by luminescence detection assay system. Real-time PCR and Western blot analysis were used to measure the expressions of RIP140 and PGC-1α genes. Results After treated with 100 nmol·L-1 AngⅡfor 36h in neonatal cardiomyocytes, the content of mitochondrial ATP was reduced notably ( P <0. 01). Accordingly, the mRNA and protein levels for RIP140 were increased. However, the mRNA and pro-tein levels of PGC-1α were downregulated markedly. What’ s more,the reduction of ATP induced by AngⅡwas further aggravated by RIP 1 4 0 overexpression , butameliorated by overexpressing PGC-1α. Conclusion The reduction of ATP mediated by AngⅡis associated with the upregulation of RIP140 , as well as the down-regulation of PGC-1α.