RIPK3-Mediated Necroptosis in Diabetic Cardiomyopathy Requires CaMKII Activation

Figure 8

Increased RIPK3 activates RIPK1 expression, MLKL phosphorylation, CaMKIIδ alternative splicing disorder, oxidation, and phosphorylation of CaMKII under diabetic conditions. I1PP1 overexpression corrects CaMKIIδ alternative splicing, inhibits CaMKII activation, and attenuates necroptosis in DCM. Taken together, CaMKII activation and necroptosis augment in diabetic cardiomyopathy via RIPK3-dependent manner.