摘要：SummaryDiabetic cardiomyopathy (DCM) is one of the most common complications of diabetes without effective treatment options. Its pathogenesis is complex and remains unclear. Long non-coding RNA (lncRNA) MIAT allele has been reported to be enriched in DCM patients and activate a pyroptosis program in hypoxia-induced H9c2 cells. Thus, whether MIAT played a role in DCM pyroptosis remains to be clarified. In the study, the expression of MIAT was found elevated in the serum of diabetic patients, as well as in high-glucose induced cardiomyocytes and diabetic mice. Further, the expression levels of CASP1 and pyroptosis correlation factors (IL-1 and IL-18) were downregulated after silencing MIAT. Through modeling and validation experiments, we then confirmed that the MIAT-miR-214-3p-CASP1 axis serves as an essential point in pyroptosis of DCM mice. These results suggested that silencing MIAT would be a potential treatment strategy for DCM.Graphical abstractDisplay OmittedHighlights•MIAT and caspase-1 were overexpressed in serum and cardiomyocytes of diabetic patients•High glucose caused inflammatory damage and calcium overloaded in cardiomyocytes•MIAT regulated pyroptosis in cardiomyocytes via MIAT-miR-214-3p-CASP1 axisClassification Description: Physiology; Cellular physiology; Molecular biology
