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Exploring the key target molecules of angiogenesis in diabetic cardiomyopathy based on bioinformatics analysis
Fengli Hu1,2, Ruixue Guo1,2, Yaxin Zhi1,2
1Department of Cardiology, Second Hospital of Hebei Medical University, Shijiazhuang, China.
Insights
Diabetic cardiomyopathy impairs cardiac microvessels. This study identifies Efnb2 as a key molecule linking angiogenesis damage to diabetic cardiomyopathy, suggesting it as a potential therapeutic target.
Area of Science:
- Cardiovascular Research
- Molecular Biology
- Diabetology
Background:
- Diabetic cardiomyopathy presents a significant clinical challenge with high incidence and severe consequences.
- Damage to cardiac microvessel angiogenesis is a critical factor in the development and progression of diabetic cardiomyopathy.
- Current treatments for diabetic cardiomyopathy lack direct targets for angiogenesis damage.
Purpose of the Study:
- To identify key molecules involved in diabetic cardiomyopathy and angiogenesis damage.
- To provide insights for potential therapeutic interventions targeting angiogenesis in diabetic cardiomyopathy.
Main Methods:
- Analysis of sequencing data from animal and cell models of diabetic cardiomyopathy.
- Functional and pathway analysis of differentially expressed angiogenesis-related genes.
- Verification of microvascular angiogenesis in diabetic mice and high glucose-stimulated human umbilical vein endothelial cells (HUVECs).
- Western blot analysis to validate top candidate genes.
Main Results:
- Identified 24 differentially expressed angiogenesis-related genes, with 11 showing consistent trends in human and mouse datasets.
- Confirmed impaired microvascular angiogenesis in diabetic mouse hearts and reduced tube formation/migration in high glucose-stimulated HUVECs.
- Efnb2 expression was significantly increased under high glucose conditions, while Edn1 and Lepr showed no significant changes.
Conclusions:
- Screened differential genes associated with angiogenesis in diabetic cardiomyopathy models.
- Elucidated a novel molecular axis linking angiogenesis damage to diabetic cardiomyopathy.
- Highlighted Efnb2 as a potential therapeutic target for diabetic cardiomyopathy.
Backgrounds:
Diabetic cardiomyopathy has a very high incidence and serious clinical consequences, making it an urgent clinical problem to be solved. Angiogenesis is a significant phenotype in the occurrence and development of diabetic cardiomyopathy, especially the damage to angiogenesis of cardiac microvessels, which is inextricably linked to the cardiac risk of diabetic patients. In the current basic and clinical research, there is still a lack of treatment methods that directly target the angiogenesis of diabetic cardiomyopathy. This study hopes to discover the key molecules related to diabetic cardiomyopathy and angiogenesis damage, to provide ideas for possible interventions.
Methods:
Sequencing data of animals and cells were obtained from the GEO database, and differentially expressed genes were analyzed. Subsequently, the angiogenesis-related genes were clustered for functional and pathway analysis. Then, the microangiogenesis of the diabetic mice and the angiogenesis changes of high glucose-stimulated HUVECs were verified, and the top three genes related to diabetic cardiomyopathy and angiogenesis were verified using western blot.
Results:
24 differentially expressed genes associated with angiogenesis were found in GSE241565(human) and GSE215979(mice). Among them, 11 genes showed the same trend in the two databases. Then CD31 staining of diabetic mice hearts showed that microvascular angiogenesis was impaired, high glucose-stimulated HUVECs decreased tube formation, and wound healing migration was weakened. Finally, the top 3 genes most associated with diabetic cardiomyopathy were verified, and there was no significant difference between the changes of Edn1 and Lepr. At the same time, Efnb2 was significantly increased under high glucose stimulation.
Conclusion:
Combined with the sequencing data of animal and cell models of diabetic cardiomyopathy, the differential genes associated with angiogenesis were screened. These findings not only elucidate a novel molecular axis linking angiogenesis damage to diabetic cardiomyopathy but also highlight Efnb2 as a potential therapeutic target.
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