TY - JOUR A2 - Brzozowski, Tomasz AU - Xing, Junhui AU - Li, Pengcheng AU - Hong, Jin AU - Wang, Mengyu AU - Liu, Yuzhou AU - Gao, Yueqiao AU - Dong, Jianzeng AU - Gu, Heping AU - Li，凌PY - 2020 DA - 2020/09/07 TI -超表达Ubiquitin-Specific蛋白酶2 (USP2)心脏抑制压力Overload-Induced心脏重塑SP - 4121750六世- 2020 AB - Ubiquitin-Specific蛋白酶2 (USP2)是一个重要的成员deubiquitination系统。GEO数据集显示，心脏压力过载时，USP2基因表达下调。然而，USP2在压力过载设置中的心肌细胞特异性功能尚不清楚。本研究采用横主动脉缩窄术(TAC, 2周)诱导小鼠压力负荷模型。AAV9感染导致USP2在心脏内过表达。采用Masson三色染色和苏木精-伊红染色(H&E)检测心脏组织学变化。超声心动图用于评估心功能。采用小麦胚芽凝集素(WGA)染色法检测心肌细胞大小。二氢乙啶染色检测心脏氧化应激。 Our results showed that USP2 was downregulated in the cardiomyocytes following 2 weeks of TAC. Overexpression of cardiac USP2 preserved ventricular function following 2 weeks of TAC. Overexpression of cardiac USP2 inhibited TAC-induced cardiac remodeling, by suppressing cardiac hypertrophy, inhibiting inflammatory responses and fibrosis, and attenuating oxidative stress. Our findings reveal a previously unrecognized role of USP2 in regulating pressure overload-induced cardiac remodeling. SN - 0962-9351 UR - https://doi.org/10.1155/2020/4121750 DO - 10.1155/2020/4121750 JF - Mediators of Inflammation PB - Hindawi KW - ER -