RIPK3-Mediated Necroptosis in Diabetic Cardiomyopathy Requires CaMKII Activation

Figure 3

RIPK3 deficiency alleviates cardiac dysfunction, CaMKIIδ alternative splicing disorder, and necroptosis in DCM. Male C57BL/6 mice and RIPK3 knockout mice (RIPK3^-/-) were injected with 60 mg/kg/d STZ for 5 consecutive days after a 12-hour overnight fast. WT and RIPK3^-/- mice in the control group were injected with the same amount of citrate buffer. (a–c) Cardiac function was assessed by echocardiography, and EF, FS, and E/A were calculated. (d) Myocardium injury was measured by HE staining.  μm. (e) cTnI was detected. (f) The mRNA levels of CaMKIIδA, CaMKIIδB, and CaMKIIδC of the myocardium were detected by quantitative real-time PCR. 18S was serviced as a housekeeping mRNA. (g) RIPK3 expression was quantified by western blot. GAPDH was used as a loading control. (h, i) Cell apoptosis of the myocardium was detected with TUNEL staining. (j, k) Cleaved-caspase 3 and caspase 3 protein expression were quantified by western blot. GAPDH was used as a loading control. and significantly from WT; ^## and # significantly from WT-DCM. .

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