Long non-coding RNA MIAT is involved in the regulation of pyroptosis in diabetic cardiomyopathy via targeting miR-214-3p

iScience

Dezhi Zheng¹  Kaiwen Deng²  Botao Yu³  Xin Chen⁴  Jun Hou⁵  Jie Ma⁶  Yonghe Hu⁶  Xudong Wen⁶  Wenjing Xiao⁷ 

[1] Department of Pharmacy, The General Hospital of Western Theater Command of PLA, No 270 Rongdu Road, Jinniu District, Chengdu 610083, China;The Third People's Hospital of Chengdu, Chengdu 610015, China;;Affiliated Hospital of Southwest Jiaotong University &Department of Cardiovascular Surgery, The 960th Hospital of the PLA Joint Logistic Support Force, Jinan 250031, China;Department of Gastroenterology and Hepatology, Chengdu First People's Hospital, Chengdu 610016, China;Department of Pharmacy, The General Hospital of Western Theater Command of PLA, No 270 Rongdu Road, Jinniu District, Chengdu 610083, China;School of Materials Science and Engineering, Southwest Jiaotong University, Chengdu 611756, China;

关键词: Classification Description: Physiology;    Cellular physiology;    Molecular biology;   

DOI  :  

来源: DOAJ

【 摘 要 】

Summary: Diabetic 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.

【 授权许可】

Unknown