Objective To study the role of telomeric repeat-binding factor 2-P53(TRF2-P53) signal pathway in diabetic cardiomyopathy.

Methods In vivo study, type 1 diabetes mouse model was induced by intraperitoneal injection of streptozocin(STZ). After 9 weeks, DCM model was successfully established. The expression level of TRF2 in mouse heart samples was detected by Western blot (WB) and P53 by immunofluorescence. In vitro studies, high sugar was given to stimulate the cardiac muscle cells of neonatal mice, TRF2 expression level was detected by WB and P53 expression level was detected by immunofluorescence. TRF2 siRNA was used to reduce the expression of TRF2 in neonatal mice cardiomyocytes, then TUNEL was used to detect apoptosis, SA-β-galactosidase (SA-β-gal) staining was used to detect condition of aging, and P53 expression level was detected by WB.

Result In vivo studies found that TRF2 expression decreased and P53 expression increased in DCM mice compared with WT mice. In vitro studies showed that high glucose stimulation caused the decrease of TRF2 expression and the increase of P53 expression in cardiomyocytes of lactating rat. TRF2 siRNA transfection can promote apoptosis and senescence and increase P53 expression after reducing TRF2 level in cardiomyocytes of lactating rat.

Conclusion TRF2-P53 signaling pathway plays an important role in the regulation of DCM.