Identification of mitophagy-related genes in patients with acute myocardial infarction

被引:0
作者
Ju-Ying Li [1 ]
Hong-Kui Chen [2 ]
Yi-Hao Huang [2 ]
Yu-Peng Zhi [3 ]
Yue-E Li [3 ]
Kai-Yang Lin [3 ]
Chun Chen [2 ]
Yan-Song Guo [3 ]
机构
[1] The First People’s Hospital of Yibin, Sichuan Province, Yibin
[2] Shenli Clincal Medical College of Fujian Medical University, Fujian Province, Fuzhou
[3] School of Pharmacy, Fujian Medical University, Fujian Province, Fuzhou
基金
中国国家自然科学基金;
关键词
Mitophagy; Acute myocardial infarction; Bioinformatic analysis; Machine learning; Gene;
D O I
10.1186/s41065-025-00424-5
中图分类号
学科分类号
摘要
Mitophagy is involved in acute myocardial infarction (AMI) process. However, the role of mitophagy-related genes (MRGs) in the AMI process is not well illustrated. We identified MRGs involved in AMI by bioinformatics analysis. The external datasets were employed for the validation of the MRGs, alongside the execution of cellular and animal experiments. Forty-five MRGs were detected, and machine learning identified the top four hub genes, namely ALDH2, ACSL1, IL1B, and GABARAPL1. Additionally, an external validation set was used to screen for three diagnostic markers (ACSL1, IL1B, and GABARAPL1) among these hub genes. Immune infiltration analysis revealed changes in the immune microenvironment among patients with AMI. Finally, the significant upregulation of ACSL1, IL1B, and GABARAPL1 in both cellular and animal models was confirmed. The occurrence of mitophagy was observed in the cell model through transmission electron microscopy (TEM). Our study demonstrated that ACSL1, IL1B, and GABARAPL1 possess potential biomarkers for AMI. © The Author(s) 2025.
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共 49 条
  • [1] Zalewski J., Nowak K., Furczynska P., Zalewska M., Complicating Acute Myocardial Infarction. Current Status and Unresolved Targets for Subsequent Research, J Clin Med, 10, 24, (2021)
  • [2] Li H., Ding J., Liu W., Wang X., Feng Y., Guan H., Et al., Plasma exosomes from patients with acute myocardial infarction alleviate myocardial injury by inhibiting ferroptosis through miR-26b-5p/SLC7A11 axis, Life Sci, 322, (2023)
  • [3] Yellon D.M., Hausenloy D.J., Myocardial reperfusion injury, N Engl J Med, 357, 11, pp. 1121-1135, (2007)
  • [4] Ajoolabady A., Chiong M., Lavandero S., Klionsky D.J., Ren J., Mitophagy in cardiovascular diseases: molecular mechanisms, pathogenesis, and treatment, Trends Mol Med, 28, 10, pp. 836-849, (2022)
  • [5] Li A., Gao M., Liu B., Qin Y., Chen L., Liu H., Et al., Mitochondrial autophagy: molecular mechanisms and implications for cardiovascular disease, Cell Death Dis, 13, 5, (2022)
  • [6] Turkieh A., El Masri Y., Pinet F., Dubois-Deruy E., Mitophagy regulation following myocardial infarction, Cells, 11, 2, (2022)
  • [7] Campos J.C., Bozi L.H., Bechara L.R., Lima V.M., Ferreira J.C., Mitochondrial quality control in cardiac diseases, Front Physiol, 7, (2016)
  • [8] Zorov D.B., Filburn C.R., Klotz L.O., Zweier J.L., Sollott S.J., Reactive oxygen species (ROS)-induced ROS release: a new phenomenon accompanying induction of the mitochondrial permeability transition in cardiac myocytes, J Exp Med, 192, 7, pp. 1001-1014, (2000)
  • [9] Gong G., Song M., Csordas G., Kelly D.P., Matkovich S.J., Dorn G.W., Parkin-mediated mitophagy directs perinatal cardiac metabolic maturation in mice, Science, 350, 6265, (2015)
  • [10] Bravo-San Pedro J.M., Kroemer G., Galluzzi L., Autophagy and mitophagy in cardiovascular disease, Circ Res, 120, 11, pp. 1812-1824, (2017)