Diabetes Exacerbates Myocardial Ischemia/Reperfusion Injury by Down-Regulation of MicroRNA and Up-Regulation of O-GlcNAcylation

Management for patients with diabetes experiencing myocardial infarction remains a challenge. Here the authors show that hyperglycemia- and hyperinsulinemia-induced microRNA-24 (miR-24) reduction and O-GlcNAcylation in the diabetic heart contribute to poor survival and increased infarct size in diab...

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Detalles Bibliográficos
Autores principales: Wang, Dandan, Hu, Xiaoyue, Lee, Seung Hee, Chen, Feng, Jiang, Kai, Tu, Zizhuo, Liu, Zejian, Du, Jing, Wang, Li, Yin, Chaoying, Liao, Yu, Shang, Hongcai, Martin, Kathleen A., Herzog, Raimund I., Young, Lawrence H., Qian, Li, Hwa, John, Xiang, Yaozu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2018
Materias:
PRECLINICAL RESEARCH
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6058960/
https://www.ncbi.nlm.nih.gov/pubmed/30062222
http://dx.doi.org/10.1016/j.jacbts.2018.01.005
Descripción
Sumario:Management for patients with diabetes experiencing myocardial infarction remains a challenge. Here the authors show that hyperglycemia- and hyperinsulinemia-induced microRNA-24 (miR-24) reduction and O-GlcNAcylation in the diabetic heart contribute to poor survival and increased infarct size in diabetic myocardial ischemia/reperfusion (I/R). In a mouse model of myocardial I/R, pharmacological or genetic overexpression of miR-24 in hearts significantly reduced myocardial infarct size. Experimental validation revealed that miR-24 targets multiple key proteins, including O-GlcNac transferase, ATG4A, and BIM, to coordinately protect the myocardium from I/R injury. These results establish miR-24 as a promising therapeutic candidate for diabetic I/R injury.

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