间充质干细胞来源的外泌体（MSCs-外泌体）被报道具有心脏保护作用。本研究探讨了MSCs-外泌体在心力衰竭（HF）治疗上的潜力和机制。使用H9c2细胞通过血管紧张素II（Ang II）处理建立心肌细胞肥大模型。通过透射电镜和CD63检测鉴定分离的MSCs-外泌体。终端脱氧核苷酸转移酶（TdT）dUTP末端标记（TUNEL）测试测量细胞凋亡率。通过ELISA测定炎症因子[白细胞介素（IL）-1β，IL-4，IL-6和肿瘤坏死因子（TNF）-α]和脑钠肽（BNP）水平。通过Western blotting检测细胞凋亡相关蛋白[Bax，B细胞淋巴瘤-2（Bcl-2）和半胱氨酸水解酶3（caspase 3）]，Hippo-YAP通路相关蛋白[YAP，磷酸（p）-YAP和tafazzin（TAZ）]的表达。MSCs-外泌体治疗改善了Ang II诱导的H9c2细胞心肌细胞肥大。MSCs-外泌体降低了Ang II诱导的H9c2细胞中Bax和caspase 3水平，并在其中升高了Bcl-2水平。MSCs-外泌体还减少了Ang II诱导的H9c2细胞中BNP，IL-1β，IL-4，IL-6和TNF-α的水平。同时，在MSCs-外泌体给药后，p-YAP下调，TAZ上调。总之，MSCs-外泌体通过关闭Hippo-YAP通路减轻心肌细胞的凋亡和炎症反应。

Mesenchymal stem cells-derived exosomes (MSCs-exosomes) reportedly possess cardioprotective effects. This study investigated the therapeutic potential and mechanisms of MSCs-exosomes on heart failure (HF). H9c2 cells were used to establish a cardiomyocyte hypertrophy model by angiotensin II (Ang II) treatment. Isolated MSCs-exosomes were identified by transmission electron microscope and CD63 detection. Apoptosis rate was measured by terminal deoxynucleotidyl transferase (TdT) dUTP Nick-End Labeling (TUNEL) assay. Levels of inflammatory factors [interleukin (IL)-1β, IL-4, IL-6, and tumor necrosis factor (TNF)-α] and brain natriuretic peptide (BNP) were determined by ELISA. Expression of apoptosis-related proteins [Bax, B-cell lymphoma-2 (Bcl-2), and caspase 3] and Hippo-Yes-associated protein (YAP) pathway-related proteins [YAP, phosphor (p)-YAP, and tafazzin (TAZ)] was detected by western blotting. Cardiomyocyte hypertrophy of H9c2 cells induced by Ang II was ameliorated by MSCs-exosomes treatment. MSCs-exosomes downregulated Bax and caspase 3 levels and upregulated Bcl-2 level in Ang II-induced H9c2 cells. MSCs-exosomes also reduced the levels of BNP, IL-1β, IL-4, IL-6, and TNF-α in Ang II-induced H9c2 cells. Meanwhile, p-YAP was downregulated and TAZ was upregulated after MSCs-exosomes administration. In conclusion, MSCs-exosomes alleviate the apoptosis and inflammatory response of cardiomyocyte via deactivating Hippo-YAP pathway in HF.