NRP1 and diabetes mellitus: These AGE’s then stimulate transmembrane receptors of advance glycation end products (rAGE) on somatic cells including cardiac myocytes resulting in alteration of intracellular signaling, gene expression, release of pro-inflammatory molecules and free radicals.19 These processes, at least in part, are thought to play a role in the development of cardiac fibrosis independent of the classic vascular complications related to diabetes mellitus.