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Accumulation of Endogenous Adenosine Improves Cardiomyocyte Metabolismvia Epigenetic Reprogramming in an Ischemia-Reperfusion Model 

Ischemic heart disease resulting from I/R injury is associated with high morbidity. Identifying cell and molecular mechanisms that contribute to cardiomyocyte death after reperfusion will be critical for development of adjunctive therapies for myocardial infarction.

In this study, we investigated the role of cellular adenosine in epigenetic regulation on cardiomyocyte gene expression, glucose metabolism and tolerance to I/R. GeneMind GenoLab M platform was used for RNA  sequencing with the aim to detect the change of ADK in the setting of I/R injury. Compared with WT group, WT mice with I/R injury had multiple changed candidate genes in ADK related pathways, while ADK was up-regulated in the setting of I/R. Further analysis revealed that ADK was significantly increased in the acute period of I/R. To sum up, the present study demonstrated that cardiomyocyte ADK deletion ameliorates myocardial I/R injury via epigenetic up-regulation of IGF-1 expression via the cardiomyocyte adenosine/DNMT1/IGF-1 axis.

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