Figure 11
From: Synergism in hyperhomocysteinemia and diabetes: role of PPAR gamma and tempol
A model for diabetic cardiomyopathy. In diabetes, elevated level of homocysteine induces oxidative radicals by antagonizing PPARγ that activates matrix metalloproteinases (MMPs), which in turn causes fibrosis and endothelial-myocytes disconnection. It results into endothelial-myocytes uncoupling that ultimately leads to diastolic dysfunction. PPARγ agonist and anti-oxidants mitigate the effect of oxidative radicals, inhibit the activity of MMPs and thereby ameliorate diastolic dysfunction.