11β-HSD1 inhibition ameliorates diabetes-induced cardiomyocyte hypertrophy and cardiac fibrosis through modulation of EGFR activity.

ABSTRACT: 11β-HSD1 has been recognized as a potential therapeutic target for type 2 diabetes. Recent studies have shown that hyperglycemia leads to activation of 11β-HSD1, increasing the intracellular glucocorticoid levels. Excess glucocorticoids may lead to the clinical manifestations of cardiac injury. Therefore, the aim of this study is to investigate whether 11β-HSD1 activation contributes to the development of diabetic cardiomyopathy. To investigate the role of 11β-HSD1, we administered a selective 11β-HSD1 inhibitor in type 1 and type 2 murine models of diabetes and in cultured cardiomyocytes. Our results show that diabetes increases cortisone levels in heart tissues. 11β-HSD1 inhibitor decreased cortisone levels and ameliorated all structural and functional features of diabetic cardiomyopathy

SUBMITTER: Zou C 

PROVIDER: S-EPMC5707098 | biostudies-literature | 2017 Nov

REPOSITORIES: biostudies-literature