Why the study?
Diabetes-induced cardiovascular complications are linked to high morbidity and mortality, and whether the cardiac risk factor IGF-IIRalpha deteriorates diabetic heart injury was unknown.
Does cardiac-specific IGF-IIRα overexpression aggravate hyperglycemia-induced cardiac inflammation and myocardial necrosis in diabetic models?
Does cardiac-specific IGF-IIRα overexpression aggravate hyperglycemia-induced cardiac inflammation and myocardial necrosis in diabetic models?
IGF-IIRα overexpression exacerbates cardiac inflammation, apoptosis, and dysfunction in diabetic models, suggesting it is a harmful factor under hyperglycemic conditions.
May position IGF-IIRα as harmful mediator in diabetic hearts; hypothesis-generating for targeted inhibition in hyperglycemia.
Diabetes-induced cardiovascular complications are mainly associated with high morbidity and mortality in patients with diabetes. Insulin-like growth factor II receptor α (IGF-IIRα) is a cardiac risk factor. In this study, we hypothesized IGF-IIRα could also deteriorate diabetic heart injury. The results presented that both in vivo transgenic Sprague-Dawley rat model with specific IGF-IIRα overexpression in the heart and in vitro myocardium H9c2 cells were used to investigate the negative function of IGF-IIRα in diabetic hearts. The results showed that IGF-IIRα overexpression aided hyperglycemia in creating more myocardial injury. Pro-inflammatory factors, such as Tumor necrosis factor-alpha, Interleukin-6, Cyclooxygenase-2, Inducible nitric oxide synthase, and Nuclear factor-kappaB inflammatory cascade, are enhanced in the diabetic myocardium with cardiac-specific IGF-IIRα overexpression. Correspondingly, IGF-IIRα overexpression in the diabetic myocardium also reduced the PI3K-AKT survival axis and activated mitochondrial-dependent apoptosis. Finally, both ejection fraction and fractional shortening were be significantly decrease in diabetic rats with cardiac-specific IGF-IIRα overexpression. Overall, all results provid clear evidence that IGF-IIRα can enhance cardiac damage and is a harmful factor to the heart under high-blood glucose conditions. However, the pathophysiology of IGF-IIRα under different stresses and its downstream regulation in the heart still require further research.
No takes yet. Share an insight, caveat, or question.
Lai et al. (2022) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: