CCR2 and diabetes mellitus: This hypothesis is supported by several pieces of evidence: infiltration of monocytes and macrophages in the hearts of models of both type 1 and type 2 diabetes (70, 71); cytokines and chemokines produced by macrophages under high glucose conditions can activate fibroblasts, promoting the secretion of fibrotic mediators and proteases (72); exosomes released by activated macrophages are considered to stimulate fibroblasts in diabetic hearts (73); genetic 3 deletion or pharmacological inhibition of the chemokine receptor CCR2 slows cardiac fibrosis in STZ-induced diabetes models (74).