β3肾上腺素能受体(Adrb3)激动剂可以激活棕色脂肪参与机体代谢，但其在高血压心肌重塑中的作用仍不清楚。我们预实验发现血管紧张素II灌注诱导的高血压模型中发生棕色脂肪功能紊乱及心肌重塑并且伴随有Adrb3表达量上升，而棕色脂肪特异性敲除Adrb3基因则加剧了心脏损伤。进一步分离培养Adrb3基因敲除小鼠的棕色脂肪细胞分泌的外泌体能够体外诱导心肌细胞的肥大。通过高通量测序及生物信息学预测等手段我们推断棕色脂肪外泌体携带的miR-200a参与了Adrb3对高血压诱导的心肌重塑的保护作用。本项目旨在此研究基础上进一步探讨：1)Adrb3改善血管紧张素II诱导的脂肪功能紊乱从而减轻高血压心脏损伤的作用；2)Adrb3调控脂肪细胞分泌功能及参与心肌损伤的分子机制；3)整体干预Adrb3及下游信号分子miR-200a对脂肪功能及高血压心肌重塑的影响，为防治高血压心脏损伤提供新的干预靶点。

β3 adrenergic receptor (Adrb3) antagonist can activate brown adipocyte and play a role in metabolism. But its role in hypertensive cardiac remodeling is not clear. We primarily found that Adrb3 expression was significantly increased in Ang II-induced hypertensive model, accompanied with induction of brown adipocyte dysfunction and cardiac remodeling. Cardiac dysfunction was aggravated in Adrb3 brown adipocyte-specific knockout mice(Adrb3-UKO) subjected to Ang II infusion. Moreover, we found that the supernatant exosomes from Adrb3-UKO brown adipocyte induced the cardiomyocyte hypertrophy. Using high-throughput sequencing and bioinformatic analysis we infer that Adrb3 regulate miR-200a of brown adipocyte exosomes and is involved in the pathology of hypertensive cardiac remodeling. The present study aimed to clarify the involvement of brown adipocyte dysfunction in cardiac remodeling and the potential mechanisms of Adrb3 regulating miR-200a during Ang II-induced hypertension. Furthermore, we will investigate whether and how Adrb3-miR-200a signaling pathway can inhibit cardiac remodeling. Our research will provide a new interference target for treatment of hypertensive cardiac injury.