Abstract：
BACKGROUND: Myocardial metabolism is closely related to functional changes after myocardial infarction (MI).
OBJECTIVE: This study aimed to present an integrative examination of human ischemic cardiomyopathy.
METHODS: 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.
RESULTS: 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.
CONCLUSIONS: This analysis provides a framework for future research on the metabolic alterations associated with MI.
OBJECTIVE: This study aimed to present an integrative examination of human ischemic cardiomyopathy.
METHODS: 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.
RESULTS: 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.
CONCLUSIONS: This analysis provides a framework for future research on the metabolic alterations associated with MI.
摘要：
背景：心肌代谢与心肌梗死（MI）后的功能变化密切相关。
目的：本研究旨在对人类缺血性心肌病进行综合检查。
方法：我们使用了GEO数据库中的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调查，我们阐明了能量代谢失调在MI进展中的关键作用。
结果：我们的发现揭示了核心调节基因CDKN1A之间的关联，FOS,ITGB4和MAP2K1与疾病的潜在病理生理学。这些基因被认为是心肌缺血疾病复杂景观中的关键元素，强调对治疗靶点和涉及的复杂生物学机制的新见解。
结论：本分析为未来研究与MI相关的代谢改变提供了框架。
目的：本研究旨在对人类缺血性心肌病进行综合检查。
方法：我们使用了GEO数据库中的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调查，我们阐明了能量代谢失调在MI进展中的关键作用。
结果：我们的发现揭示了核心调节基因CDKN1A之间的关联，FOS,ITGB4和MAP2K1与疾病的潜在病理生理学。这些基因被认为是心肌缺血疾病复杂景观中的关键元素，强调对治疗靶点和涉及的复杂生物学机制的新见解。
结论：本分析为未来研究与MI相关的代谢改变提供了框架。
