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Modeling and Evaluation of Murine Diabetic Cardiomyopathy Model
Published on: November 29, 2024
CD226 deficiency attenuates cardiac early pathological remodeling and dysfunction via decreasing inflammatory
Yongli Hou1, Yazhen Wang1, Kang Tang1
1Department of Immunology, Fourth Military Medical University, Xi'an, China.
Insights
CD226 promotes inflammation and cardiac dysfunction in diabetic cardiomyopathy (DCM) by activating macrophages. CD226 deficiency improves heart function and reduces macrophage glycolysis, offering a potential therapeutic target for DCM.
Area of Science:
- Cardiovascular Research
- Immunology
- Metabolic Diseases
Background:
- Diabetic cardiomyopathy (DCM) is a significant complication of type 1 diabetes.
- Activated macrophages play a crucial role in DCM-associated inflammation.
- The specific role of CD226 in macrophage function during DCM progression requires elucidation.
Purpose of the Study:
- To investigate the role of CD226 in macrophage function in the context of diabetic cardiomyopathy.
- To determine the impact of CD226 on cardiac dysfunction and macrophage behavior in a mouse model of diabetes.
Main Methods:
- Utilized streptozotocin (STZ)-induced diabetes mouse model.
- Analyzed cardiac macrophage populations and CD226 expression levels.
- Investigated the effects of CD226 deficiency and bone marrow-derived macrophage (BMDM) transfer on cardiac function and macrophage metabolism.
Main Results:
- STZ-induced diabetes increased cardiac macrophage numbers and CD226 expression.
- CD226 deficiency attenuated diabetes-induced cardiac dysfunction and reduced CD86+ F4/80+ macrophage proportion.
- Adoptive transfer of CD226-deficient BMDMs alleviated cardiac dysfunction, linked to reduced macrophage migration under high glucose.
- CD226 deficiency decreased macrophage glycolysis, downregulating Hexokinase 2 (HK2) and Lactate Dehydrogenase A (LDH-A) expression.
Conclusions:
- CD226 plays a pathogenic role in diabetic cardiomyopathy by promoting macrophage activation, migration, and glycolysis.
- Targeting CD226 may offer a novel therapeutic strategy for treating diabetic cardiomyopathy.
Abstract:
Diabetic cardiomyopathy (DCM) is one of the main complications in type I diabetic patients. Activated macrophage is critical for directing the process of inflammation during the development of DCM. The present study focused on the roles of CD226 on macrophage function during the DCM progression. It has been found that the number of cardiac macrophages in the hearts of streptozocin (STZ)-induced diabetes mice was significantly increased compared with that in non-diabetes mice, and the expression level of CD226 on cardiac macrophages in STZ-induced diabetes mice was higher than that in non-diabetes mice. CD226 deficiency attenuated the diabetes-induced cardiac dysfunction and decreased the proportion of CD86+ F4/80+ macrophages in the diabetic hearts. Notably, adoptive transfer of Cd226-/- - bone marrow derived macrophages (BMDMs) alleviated diabetes-induced cardiac dysfunction, which may be due to the attenuated migration capacity of Cd226-/- -BMDM under high glucose stimulation. Furthermore, CD226 deficiency decreased the macrophage glycolysis accompanying by the downregulated hexokinase 2 (HK2) and lactate dehydrogenase A (LDH-A) expression. Taken together, these findings revealed the pathogenic roles of CD226 played in the process of DCM and provided a basis for the treatment of DCM.
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