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Platelet mitochondrial DNA methylation : A novel biomarker for myocardial infarction – A preliminary study

Peng, Ningxin ; Guo, Liqiong ; Wei, Zhonghai ; Wang, Xiao LU ; Zhao, Lei ; Kang, Lina ; Wang, Kun LU ; Zhou, Weihong ; Cheng, Shoujun and Yin, Songjiang LU , et al. (2023) In International Journal of Cardiology
Abstract

Background: Platelet activation and thrombus formation play critical roles in the pathogenesis of myocardial infarction (MI). In addition to their role in energy production, platelet mitochondria also regulate cellular functions related to apoptosis, oxidative stress, and inflammation. Epigenetic modifications of platelet mitochondrial DNA (mtDNA) may influence platelet function and are believed to be an important factor in MI. Therefore, the aim of this study was to investigate the differences in platelet mtDNA methylation levels between MI patients and controls. Methods: The present study utilized propensity score matching to generate 45 multivariate matched apparently healthy controls for 45 patients with newly-onset acute MI.... (More)

Background: Platelet activation and thrombus formation play critical roles in the pathogenesis of myocardial infarction (MI). In addition to their role in energy production, platelet mitochondria also regulate cellular functions related to apoptosis, oxidative stress, and inflammation. Epigenetic modifications of platelet mitochondrial DNA (mtDNA) may influence platelet function and are believed to be an important factor in MI. Therefore, the aim of this study was to investigate the differences in platelet mtDNA methylation levels between MI patients and controls. Methods: The present study utilized propensity score matching to generate 45 multivariate matched apparently healthy controls for 45 patients with newly-onset acute MI. Platelet mtDNA methylation levels were assessed through bisulfite-PCR pyrosequencing and compared between the two groups, with further adjustments made in the sensitivity analysis. Results: Among the measured mitochondrial genes (MT-COX1, MT-COX2, MT-COX3, MT-ND5, MT-ATP6 and tRNA_Leu), patients with MI exhibited statistically significant differences in mtDNA methylation levels as compared to matched controls. Specifically, higher levels of mtDNA methylation were observed in MT-COX1, MT-COX3, and tRNA_Leu, while a lower level was observed in MT-ATP6 (all p < 0.0001). These results remained robust in the sensitivity analysis. Conclusion: Our study demonstrated significant variations in platelet mtDNA methylation levels between patients with MI and controls. Platelet mtDNA methylation may serve as a novel biomarker for MI. This observation also provided some insights into the etiology of MI.

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organization
publishing date
type
Contribution to journal
publication status
in press
subject
keywords
Mitochondrial DNA methylation, Myocardial infarction, Platelet
in
International Journal of Cardiology
article number
131606
publisher
Elsevier
external identifiers
  • pmid:37996014
  • scopus:85178000745
ISSN
0167-5273
DOI
10.1016/j.ijcard.2023.131606
language
English
LU publication?
yes
additional info
Funding Information: The authors thank all participants of the study and the staff of the Department of Cardiology of Nanjing Drum Tower Hospital and the Department of Health Management Center of Nanjing Drum Tower Hospital. Funding Information: The present study was funded by the Natural Science Foundation of Jiangsu Province (BK20200128 and BK20200842), the Nanjing Medical Science and Technology Development Project (YKK21070), the National Natural Science Foundation of China (82100478), and the Jiangsu Planned Projects for Postdoctoral Research Funds (2021K287B). Publisher Copyright: © 2023 Elsevier B.V.
id
4acff17d-c986-4c1e-a05d-b3b91510f7f9
date added to LUP
2024-01-08 14:24:09
date last changed
2024-05-21 13:16:29
@article{4acff17d-c986-4c1e-a05d-b3b91510f7f9,
  abstract     = {{<p>Background: Platelet activation and thrombus formation play critical roles in the pathogenesis of myocardial infarction (MI). In addition to their role in energy production, platelet mitochondria also regulate cellular functions related to apoptosis, oxidative stress, and inflammation. Epigenetic modifications of platelet mitochondrial DNA (mtDNA) may influence platelet function and are believed to be an important factor in MI. Therefore, the aim of this study was to investigate the differences in platelet mtDNA methylation levels between MI patients and controls. Methods: The present study utilized propensity score matching to generate 45 multivariate matched apparently healthy controls for 45 patients with newly-onset acute MI. Platelet mtDNA methylation levels were assessed through bisulfite-PCR pyrosequencing and compared between the two groups, with further adjustments made in the sensitivity analysis. Results: Among the measured mitochondrial genes (MT-COX1, MT-COX2, MT-COX3, MT-ND5, MT-ATP6 and tRNA_Leu), patients with MI exhibited statistically significant differences in mtDNA methylation levels as compared to matched controls. Specifically, higher levels of mtDNA methylation were observed in MT-COX1, MT-COX3, and tRNA_Leu, while a lower level was observed in MT-ATP6 (all p &lt; 0.0001). These results remained robust in the sensitivity analysis. Conclusion: Our study demonstrated significant variations in platelet mtDNA methylation levels between patients with MI and controls. Platelet mtDNA methylation may serve as a novel biomarker for MI. This observation also provided some insights into the etiology of MI.</p>}},
  author       = {{Peng, Ningxin and Guo, Liqiong and Wei, Zhonghai and Wang, Xiao and Zhao, Lei and Kang, Lina and Wang, Kun and Zhou, Weihong and Cheng, Shoujun and Yin, Songjiang and Xu, Biao and Bao, Xue}},
  issn         = {{0167-5273}},
  keywords     = {{Mitochondrial DNA methylation; Myocardial infarction; Platelet}},
  language     = {{eng}},
  publisher    = {{Elsevier}},
  series       = {{International Journal of Cardiology}},
  title        = {{Platelet mitochondrial DNA methylation : A novel biomarker for myocardial infarction – A preliminary study}},
  url          = {{http://dx.doi.org/10.1016/j.ijcard.2023.131606}},
  doi          = {{10.1016/j.ijcard.2023.131606}},
  year         = {{2023}},
}