Key result
Circ_0002295 promotes myocardial fibrosis progression by sponging miR-1287 to upregulate CXCR2.
Why the study?
Circular RNA is reported to be a key regulatory factor of myocardial fibrosis progression, which is involved in hypertension, myocardial infarction, and heart failure.
Does knockdown of circ_0002295 prevent myocardial fibrosis progression in cardiac myofibroblasts?
Does knockdown of circ_0002295 prevent myocardial fibrosis progression in cardiac myofibroblasts?
Circ_0002295 promotes myocardial fibrosis progression through the miR-1287/CXCR2 axis, suggesting a potential therapeutic target for myocardial fibrosis.
Supports circ_0002295 inhibition in animal fibrosis models; leaves open human therapeutic relevance.
Myocardial fibrosis (MF) is involved in hypertension, myocardial infarction and heart failure. It has been reported that circular RNA (circRNA) is a key regulatory factor of MF progression. In this study, we revealed that circ_0002295 and CXCR2 were elevated, and miR-1287 was reduced in MF patients. Knockdown of circ_0002295 effectively suppressed the proliferation, migration and MF progression. Circ_0002295 was the molecular sponge of miR-12878, and miR-1287 inhibitor reversed the biological functions of circ_0002295 on the myocardial fibrosis. CXCR2 was a target gene of miR-1287, and CXCR2 silencing relieved the impacts of miR-1287 inhibitor on cardiac myofibroblasts. Circ_0002295 promoted MF progression by regulating the miR-1287/CXCR2 axis, providing a possible circRNA-targeted therapy for MF.
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Ma et al. (2023) studied Myocardial fibrosis. circ_0002295 was evaluated on Myocardial fibrosis progression. Circ_0002295 promoted myocardial fibrosis progression by acting as a molecular sponge for miR-1287 to upregulate CXCR2.
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