A Novel Disulfidptosis-Related Diagnostic Gene Signature and Differential Expression Validation in Ischaemic Cardiomyopathy

IF 5.3
Xin Tan, Shuai Xu, Yiyao Zeng, Fengyi Yu, Zhen Qin, Ge Zhang, Jili Fan, Xiaohong Bo, Junnan Tang, Huimin Fan, Yafeng Zhou
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引用次数: 0

Abstract

Ischaemic cardiomyopathy (IC) predominantly arises from prolonged deprivation of oxygen in the coronary arteries, resulting in compromised cardiac contractility or relaxation. This study investigates the role of disulfidptosis-associated genes (DiGs) in IC. Through the analysis of datasets GSE5406 and GSE57338, we explored the association between DiGs and immune characteristics to identify crucial genes contributing to IC development. The support vector machine model emerged as the most effective, identifying key genes such as MYH9, NUBPL, MYL6, MYH10 and NCKAP1. Validation with independent datasets GSE57345, GSE48166 and single-cell GSE145154 further supported these findings, demonstrating high predictive accuracy. Experimental validation in an IC mouse model, using Western blot, immunohistochemistry and RT-qPCR, confirmed the altered expression of these core genes in myocardial ischaemic regions. This research not only elucidates the significance of DiGs in IC but also underscores the diagnostic potential of identified core genes.

Abstract Image

缺血性心肌病中一种新的二硫中毒相关诊断基因标记和差异表达验证
缺血性心肌病(IC)主要是由冠状动脉长期缺氧引起的,导致心脏收缩性或舒张性受损。本研究探讨了二硫中毒相关基因(DiGs)在IC中的作用。通过分析数据集GSE5406和GSE57338,我们探讨了DiGs与免疫特性之间的关系,以确定促进IC发展的关键基因。支持向量机模型是最有效的,可以识别出MYH9、NUBPL、MYL6、MYH10和NCKAP1等关键基因。独立数据集GSE57345、GSE48166和单细胞数据集GSE145154的验证进一步支持了这些发现,显示出较高的预测准确性。在IC小鼠模型中,通过Western blot、免疫组织化学和RT-qPCR的实验验证,证实了这些核心基因在心肌缺血区域的表达改变。本研究不仅阐明了DiGs在IC中的重要意义,而且强调了鉴定出的核心基因的诊断潜力。
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来源期刊
CiteScore
11.50
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0.00%
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期刊介绍: The Journal of Cellular and Molecular Medicine serves as a bridge between physiology and cellular medicine, as well as molecular biology and molecular therapeutics. With a 20-year history, the journal adopts an interdisciplinary approach to showcase innovative discoveries. It publishes research aimed at advancing the collective understanding of the cellular and molecular mechanisms underlying diseases. The journal emphasizes translational studies that translate this knowledge into therapeutic strategies. Being fully open access, the journal is accessible to all readers.
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