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标题：Celecoxib alleviates pathological cardiac hypertrophy and fibrosis via M1-like macrophage infiltration in neonatal mice
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作者：Yanli Zhao ; Qi Zheng ; Hanchao Gao 等
期刊名称：iScience
印刷版ISSN：2589-0042
出版年度：2021
卷号：24
期号：3
页码：1-24
DOI：10.1016/j.isci.2021.102233
语种：English
出版社：Elsevier
摘要：SummaryCardiac hypertrophy is an adaptive response to all forms of heart disease, including hypertension, myocardial infarction, and cardiomyopathy. Cyclooxygenase-2 (COX-2) overexpression results in inflammatory response, cardiac cell apoptosis, and hypertrophy in adult heart after injury. However, immune response-mediated cardiac hypertrophy and fibrosis have not been well documented in injured neonatal heart. This study showed that cardiac hypertrophy and fibrosis are significantly attenuated in celecoxib (a selective COX-2 inhibitor)-treated P8 ICR mice after cryoinjury. Molecular and cellular profiling of immune response shows that celecoxib inhibits the production of cytokines and the expression of adhesion molecular genes, increases the recruitment of M1-like macrophage at wound site, and alleviates cardiac hypertrophy and fibrosis. Furthermore, celecoxib administration improves cardiac function at 4 weeks after injury. These results demonstrate that COX-2 inhibition promotes the recruitment of M1-like macrophages during early wound healing, which may contribute to the suppression of cardiac hypertrophy and fibrosis after injury.Graphical abstractDisplay OmittedHighlights•Cryoinjury successfully induces cardiac hypertrophy and fibrosis in P8 ICR mice•COX-2 inhibition alleviates cardiac hypertrophy and fibrosis after cryoinjury•MCP-1 significantly increases in COX-2 inhibition•COX-2 inhibition improves cardiac repair in P8 ICR mice by recruiting M1-like macrophagesAnimal Physiology; Molecular Physiology; Molecular Biology