Type 1 and type 2 diabetes in mice worsened cardiac dysfunction after myocardial infarction with increased wall thinning and decreased ejection fraction despite similar infarct sizes compared to non-diabetic mice.
Do type 1 and type 2 diabetes produce distinct immunometabolic signatures and cardiac remodeling patterns in a murine model of myocardial infarction?
Type 1 and Type 2 diabetes drive distinct inflammatory, metabolic, and structural responses following myocardial infarction, suggesting that tailored therapeutic strategies may be required for different diabetic phenotypes.
DM promotes adverse cardiac remodeling, which is associated with activation of overlapping and unique inflammatory pathways, impaired ECM remodeling, remote metabolic remodeling, and alterations in macrophage metabolism. Our results provide novel insights into potential therapeutic pathways for DM patients suffering from MI.
O’Quinn et al. (Sun,) conducted a other in Adult male C57BL/6J mice aged 16-20 weeks with type 1 diabetes induced by single high-dose streptozotocin or type 2 diabetes induced by high-fat/fructose diet plus multiple low-dose streptozotocin and myocardial infarction by permanent coronary artery ligation. Type 1 diabetes induction by single high-dose STZ and Type 2 diabetes induction by high-fat/fructose diet plus multiple low-dose STZ vs. Non-diabetic control mice with saline injection and normal diet was evaluated on Left ventricular (LV) structural remodeling and function including infarct wall thickness, ejection fraction, LV volumes at days 0, 3, 7, and 28 post-MI. Type 1 and type 2 diabetes in mice worsened cardiac dysfunction after myocardial infarction with increased wall thinning and decreased ejection fraction despite similar infarct sizes compared to non-diabetic mice.