Endocrine, metabolic & immune disorders drug targets · 2026
An Integrative Analysis of the Role of Mitophagy in Comorbid Myocardial Infarction and Type 2 Diabetes Mellitus.
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Yang Ying, Wan Feiyan, Xu Xuelian, Xu Wei, Jiang Lingli, Pan Pei
Аннотация
INTRODUCTION: Coexisting myocardial infarction (MI) and type 2 diabetes mellitus (T2DM) is a common condition. We aimed to investigate the association between MI and type 2 diabetes (T2D) with mitophagy-related differentially expressed genes (MRDEGs) and the impact thereof on disease progression.
METHODS: R package was used for data retrieval and normalization of the MI (GSE48060 and GSE29532) and T2D (GSE76894 and GSE25724) datasets. Gene set enrichment analysis indicated significant associations between biological functions and pathways. Protein-protein interaction networks constructed using STRING and GeneMANIA revealed interconnected MRDEGs.
RESULTS: Principal component and differential gene expression analyses identified 45 MRDEGs. Through key gene screening, least absolute shrinkage, and selection operator (LASSO) risk model construction, nine MRDEGs were identified: ATG14, BIRC2, CSK, FBXO7, HNRNPH1, HNRNPL, SNX6, TFEB, and YES1M. A diagnostic nomogram model exhibited high reliability and validity when utilizing these genes. Using LASSO regression analysis, the risk score formula demonstrated diagnostic accuracy for MI and T2D.
DISCUSSION: This study highlights the significance of immune cell infiltration in the context of MI and T2D. This analysis is primarily based on publicly available datasets, and future research will incorporate independent patient cohorts to assess the role of mitochondrial autophagy in these diseases.
CONCLUSION: The screened genes may be therapeutic targets to prevent progression and improve clinical outcomes in patients with MI and T2D. This study provides an integrative view of mitochondrial metabolism and immune infiltration in MI and T2D, offering a novel direction to further elucidate the pathogenesis and medical interventions for these diseases.
METHODS: R package was used for data retrieval and normalization of the MI (GSE48060 and GSE29532) and T2D (GSE76894 and GSE25724) datasets. Gene set enrichment analysis indicated significant associations between biological functions and pathways. Protein-protein interaction networks constructed using STRING and GeneMANIA revealed interconnected MRDEGs.
RESULTS: Principal component and differential gene expression analyses identified 45 MRDEGs. Through key gene screening, least absolute shrinkage, and selection operator (LASSO) risk model construction, nine MRDEGs were identified: ATG14, BIRC2, CSK, FBXO7, HNRNPH1, HNRNPL, SNX6, TFEB, and YES1M. A diagnostic nomogram model exhibited high reliability and validity when utilizing these genes. Using LASSO regression analysis, the risk score formula demonstrated diagnostic accuracy for MI and T2D.
DISCUSSION: This study highlights the significance of immune cell infiltration in the context of MI and T2D. This analysis is primarily based on publicly available datasets, and future research will incorporate independent patient cohorts to assess the role of mitochondrial autophagy in these diseases.
CONCLUSION: The screened genes may be therapeutic targets to prevent progression and improve clinical outcomes in patients with MI and T2D. This study provides an integrative view of mitochondrial metabolism and immune infiltration in MI and T2D, offering a novel direction to further elucidate the pathogenesis and medical interventions for these diseases.