Wang Zongtao, Xie Zhixin, Li Tudi, Chen Rong, Zeng Zhihuan, Guo Jun
Department of Cardiology, The First Affiliated Hospital of Jinan University, Guangzhou, 510630, China.
Department of Cardiology, The First Affiliated Hospital of Guangdong Pharmaceutical University, Guangzhou, 510080, China.
Curr Vasc Pharmacol. 2025;23(1):57-66. doi: 10.2174/0115701611289159240724114844.
Myocardial metabolism is closely related to functional changes after myocardial infarction (MI).
This study aimed to present an integrative examination of human ischemic cardiomyopathy.
We used both GSE121893 single-cell suspension sequencing and GSE19303 transcription microarray data sets from the GEO database, along with a murine MI model for full-spectrum metabolite detection. Through a systematic investigation that involved differential metabolite identification and functional enrichment analysis, we shed light on the pivotal role of energy metabolism dysregulation in the progression of MI.
Our findings revealed an association between the core regulatory genes CDKN1A, FOS, ITGB4, and MAP2K1 and the underlying pathophysiology of the disease. These genes are identified as critical elements in the complex landscape of myocardial ischemic disorder, highlighting novel insights into therapeutic targets and the intricate biological mechanisms involved.
This analysis provides a framework for future research on the metabolic alterations associated with MI.
心肌代谢与心肌梗死(MI)后的功能变化密切相关。
本研究旨在对人类缺血性心肌病进行综合检查。
我们使用了来自GEO数据库的GSE121893单细胞悬浮测序和GSE19303转录微阵列数据集,以及用于全谱代谢物检测的小鼠MI模型。通过涉及差异代谢物鉴定和功能富集分析的系统研究,我们揭示了能量代谢失调在MI进展中的关键作用。
我们的研究结果揭示了核心调节基因CDKN1A、FOS、ITGB4和MAP2K1与该疾病潜在病理生理学之间的关联。这些基因被确定为心肌缺血性疾病复杂格局中的关键要素,突出了对治疗靶点和所涉及的复杂生物学机制的新见解。
该分析为未来关于MI相关代谢改变的研究提供了一个框架。