期刊
MOLECULAR THERAPY-NUCLEIC ACIDS
卷 17, 期 -, 页码 636-643出版社
CELL PRESS
DOI: 10.1016/j.omtn.2019.06.026
关键词
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资金
- National Natural Science Foundation of China [81770809, 81673426]
- Bethune-Merck Diabetes Research Foundation [G2017044]
- Graduate Innovation Fund of Harbin Medical University [YJSCX2017-59HYD]
Diabetic cardiomyopathy (DCM) is a vital cause of fatalities in diabetic patients. The programmed death of cardiomyocytes and inflammation critically contribute to cardiac hypertrophy and fibrosis in DCM. Furthermore, circular RNA (circRNA) is a key regulator of various diseases. However, the role of circRNAs inDCMremains to be elucidated. Our previous study found that pyroptosis was markedly activated in the cardiomyocytes subjected to high-glucose conditions, and miR-214-3p regulated the expression of caspase-1. The aim of this study was to elucidate whether circRNA is involved in DCM pyroptosis via the miR-214-3p/caspase-1 pathway. Herein, we identified that hsa_circ_0076631, named caspase-1-associated circRNA (CACR), was increased both in high-glucose-treated cardiomyocytes and in the serum of diabetic patients. CACR also sponged an endogenous miR-214-3p to sequester and inhibit its expression. CACR knockdown in cardiomyocytes counteracted high-glucose-induced caspase-1 activation. Conversely, miR-214-3p knockdown partially abolished the beneficial effects of CACR silencing on pyroptosis in cardiomyocytes. Therefore, this study elucidated that CACRmight be a novel therapeutic target via the CACR/miR-214-3p/caspase-1 pathway in DCM.
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