Additional file 1 of Aerobic exercise training attenuates cardiac inflammation and fibrosis in mice with type 2 diabetes and inhibits the advanced glycation end products pathway

Supplementary Material 1: Figure 1: Mechanistic representation of the AGE-RAGE signaling pathway in the context of type 2 diabetes (T2D). Hyperglycemia leads to increased glucose flux through metabolic pathways such as polyol, hexosamine and glycolysis, resulting in oxidative stress, mitochondrial dysfunction and activation of inflammatory signaling. The accumulation of advanced glycation end products (AGEs) and their interaction with the receptor for AGEs (RAGE) trigger downstream signaling pathways involving oxidative phosphorylation overload, ER stress, apoptosis and fibrosis. These mechanisms culminate in structural and functional changes in the heart, including myocardial inflammation and fibrosis and vascular myocardial dysfunction.