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CTRP3 attenuates cardiac dysfunction, inflammation, oxidative stress and cell death in diabetic cardiomyopathy in
Zhen-Guo Ma1,2,3, Yu-Pei Yuan1,2,3, Si-Chi Xu1,2,3
1Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan University, Jiefang Road 238, Wuhan, 430060, People's Republic of China.
Aims/Hypothesis:
Oxidative stress, inflammation and cell death are closely involved in the development of diabetic cardiomyopathy (DCM). C1q/tumour necrosis factor-related protein-3 (CTRP3) has anti-inflammatory properties but its role in DCM remains largely unknown. The aims of this study were to determine whether CTRP3 could attenuate DCM and to clarify the underlying mechanisms.
Methods:
Streptozotocin (STZ) was injected intraperitoneally to induce diabetes in Sprague-Dawley rats. Cardiomyocyte-specific CTRP3 overexpression was achieved using an adeno-associated virus system 12 weeks after STZ injection.
Results:
CTRP3 expression was significantly decreased in diabetic rat hearts. Knockdown of CTRP3 in cardiomyocytes at baseline resulted in increased oxidative injury, inflammation and apoptosis in vitro. Cardiomyocyte-specific overexpression of CTRP3 decreased oxidative stress and inflammation, attenuated myocyte death and improved cardiac function in rats treated with STZ. CTRP3 significantly activated AMP-activated protein kinase α (AMPKα) and Akt (protein kinase B) in H9c2 cells. CTRP3 protected against high-glucose-induced oxidative stress, inflammation and apoptosis in vitro. AMPKα deficiency abolished the protective effects of CTRP3 in vitro and in vivo. Furthermore, we found that CTRP3 activated AMPKα via the cAMP-exchange protein directly activated by cAMP (EPAC)-mitogen-activated protein kinase kinase (MEK) pathway.
Conclusions/Interpretation:
CTRP3 protected against DCM via activation of the AMPKα pathway. CTRP3 has therapeutic potential for the treatment of DCM.
Insights
C1q/tumour necrosis factor-related protein-3 (CTRP3) protects against diabetic cardiomyopathy (DCM) by reducing oxidative stress and inflammation. CTRP3 activates the AMP-activated protein kinase alpha (AMPKα) pathway, offering potential therapeutic benefits for DCM.
Area of Science:
- Cardiovascular Biology
- Metabolic Diseases
- Molecular Mechanisms
Background:
- Diabetic cardiomyopathy (DCM) involves oxidative stress, inflammation, and cell death.
- C1q/tumour necrosis factor-related protein-3 (CTRP3) possesses anti-inflammatory properties, but its role in DCM is unclear.
Purpose of the Study:
- To investigate the potential of CTRP3 in attenuating DCM.
- To elucidate the underlying mechanisms of CTRP3's action in DCM.
Main Methods:
- Diabetes was induced in Sprague-Dawley rats using streptozotocin (STZ).
- Cardiomyocyte-specific CTRP3 overexpression was achieved via adeno-associated virus vectors.
- In vitro studies utilized H9c2 cells to assess CTRP3's effects on high-glucose-induced stress.
Main Results:
- CTRP3 expression was reduced in diabetic rat hearts.
- CTRP3 overexpression decreased oxidative stress, inflammation, and myocyte death, improving cardiac function in STZ-treated rats.
- CTRP3 activated AMP-activated protein kinase alpha (AMPKα) and Akt, with AMPKα activation being crucial for its protective effects.
Conclusions:
- CTRP3 protects against DCM through the activation of the AMPKα pathway.
- CTRP3 demonstrates significant therapeutic potential for treating diabetic cardiomyopathy.
