Author + information
- Yupei Yuan and
- Qizhu Tang
Diabetic cardiomyopathy is defined as left ventricular dysfunction that occurs in diabetic patients independent of hypertension and coronary artery disease. Previous studies have highlighted the importance of oxidative stress, inflammation, myocardial fibrosis, and cell apoptosis in the process of diabetic cardiomyopathy. It's reported that C1q/TNF related protein 3 (CTRP3), a newly identified adipokine, could inhibit inflammatory response and cell apoptosis. However, the role of CTRP3 in diabetic cardiomyopathy is still unclear.
The rats were intraperitoneally injected with streptozotocin (STZ) (65mg/kg) once to induce diabetes. Twelve weeks after STZ injection, heart function was evaluated by echocardiography. Subsequently, adeno-associated virus 9 overexpressing CTRP3 (AAV-CTRP3) was intramyocardially injected into the animals with diabetes. Echocardiography and hemodynamic analysis were performed after 6 weeks post AAV-CTRP3 injection. Heart weight (HW) and tibia length (TL) were also examined. HE and PSR staining were used to observe cell area and cardiac fibrosis. Immunohistochemistry were used to detect the levels of TNF-α. Western blot and immunofluorescence were applied to determine expressions of proteins. TUNEL was used to assay apoptosis.
Increased echocardiographic parameters and restored dp/dt were observed after AAV-CTRP3 injection. CTRP3 also increased HW and HW/TL. CTRP3 limited STZ-induced cardiac fibrosis, as indicated by decreased collagen volume, reduced fibrotic markers and diminished level of CTGF. CTRP3 also attenuated STZ-induced cell apoptosis in the heart, as reflected by the decreased numbers of TUNEL positive cells and the changes of apoptosis-associated proteins. CTRP3 also reduced the levels of TNF-α confirmed by western and immunohistochemistry.
Overexpression of CTRP3 in heart attenuates STZ-induced cardiac injury.