期刊论文

Jiang, ZS

英文

European Journal of Pharmacology

0014-2999

2023

949

175735

10.1016/j.ejphar.2023.175735

CRediT authorship contribution statement HuiTing Liu: Conducted the experiments, Formal analysis, Writing – original draft. ZhiXiang Zhou: Data curation. HuaNian Deng: Data curation. Zhen Tian: Data curation. ZeFan Wu: Writing – review & editing. XiYan Liu: Writing – review & editing. Zhong Ren: Writing – review & editing. ZhiSheng Jiang: Conceptualization, acquisition, Resources, Supervision, Review, All authors have read and approved the final manuscript. Acknowledgments Trim65-KO mice were kind gifts from the Professor Zhou Rongbin (University of Science and Technology of China). This research was funded by the National Key Research and Development Program of China (2019YFA0801601 to ZSJ), the National Natural Science Foundation of China (91839103, 81670429, to ZSJ), Special for Construction of Innovative Provinces in Hunan Province (2020SK2105 to ZSJ), International Joint Laboratory for Arteriosclerotic Disease Research of Hunan Province (2018WK4031),

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Pathological cardiac hypertrophy is a major cause of heart failure, and there is no effective approach for its prevention or treatment. The Trim family is a recently identified family of E3 ubiquitin ligases that regulate cardiac hypertrophy. Trim65, which is a member of the Trim family, previous studies have not determined whether Trim65 affects cardiac hypertrophy. In this study, the effects of Trim65 on isoproterenol (ISO)-induced cardiac hypertrophy and the underlying mechanisms were investigated. In contrast to C57BL/6 mice, Trim65-knockout (Trim65-KO) mice developed more severe myocardia...