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Peer-reviewedCC BY 4.0International Journal of Molecular Sciences

Evolutionary Epigenetic Analysis of Oxidative Balance Score-Associated DNA Methylation Sites Across Mammals

  • Sun-Young Kang1
  • Jeong-Soo Gim2
  • Kyung-Wan Baek3
  • Jeong-An Gim1,4
4 affiliations
  1. 1Institute for Molecular Metabolism Innovation, Soonchunhyang University, Asan 31538, Republic of Korea
  2. 2Department of Pet Health Care, Busan Health University, Busan 49318, Republic of Korea
  3. 3Research Institute of Pharmaceutical Sciences, Gyeongsang National University, Jinju 52828, Republic of Korea
  4. 4Department of Medical Science, Soonchunhyang University, Asan 31538, Republic of Korea
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Abstract

Oxidative Balance Score (OBS) summarizes diet- and lifestyle-related exposures relevant to redox homeostasis, but the evolutionary behavior of OBS-associated epigenetic markers remains unclear. In this study, we conducted a covariate-adjusted epigenome-wide association study (EWAS) in Korean Genome and Epidemiology Study (KoGES) cohorts, adjusting for OBS and cell-type proportions. We identified 26 robust OBS-associated CpG sites. We then mapped these loci to the Mammalian Methylation Consortium dataset (GSE223748) and examined age-related methylation dynamics across nine mammalian species, using chronological age as a proxy for cumulative oxidative burden. Cross-species analyses showed that human correlation patterns were only partially preserved, with greater concordance observed in primates than in several non-primate species. Furthermore, 1000-iteration bootstrap resampling and null-model sensitivity analyses (Robinson-Foulds distance) demonstrated that the interspecies clustering topology of these 26 CpGs is statistically robust and distinct from random genomic noise. These findings suggest partial evolutionary preservation of age-related methylation behavior at human OBS-associated loci, providing a comparative framework for redox-related epigenetic dynamics.

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Cite

BibTeXRIS
BibTeX
@article{kang2026evolutionary,
  title = {{Evolutionary Epigenetic Analysis of Oxidative Balance Score-Associated DNA Methylation Sites Across Mammals}},
  author = {Sun-Young Kang and Jeong-Soo Gim and Kyung-Wan Baek and Jeong-An Gim},
  journal = {International Journal of Molecular Sciences},
  year = {2026},
  month = sep,
  doi = {10.3390/ijms27198772},
  url = {https://www.mdpi.com/1422-0067/27/19/8772},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Evolutionary Epigenetic Analysis of Oxidative Balance Score-Associated DNA Methylation Sites Across Mammals
AU  - Sun-Young Kang
AU  - Jeong-Soo Gim
AU  - Kyung-Wan Baek
AU  - Jeong-An Gim
PY  - 2026
DA  - 2026/09/30
JO  - International Journal of Molecular Sciences
DO  - 10.3390/ijms27198772
UR  - https://www.mdpi.com/1422-0067/27/19/8772
AB  - Oxidative Balance Score (OBS) summarizes diet- and lifestyle-related exposures relevant to redox homeostasis, but the evolutionary behavior of OBS-associated epigenetic markers remains unclear. In this study, we conducted a covariate-adjusted epigenome-wide association study (EWAS) in Korean Genome and Epidemiology Study (KoGES) cohorts, adjusting for OBS and cell-type proportions. We identified 26 robust OBS-associated CpG sites. We then mapped these loci to the Mammalian Methylation Consortium dataset (GSE223748) and examined age-related methylation dynamics across nine mammalian species, using chronological age as a proxy for cumulative oxidative burden. Cross-species analyses showed that human correlation patterns were only partially preserved, with greater concordance observed in primates than in several non-primate species. Furthermore, 1000-iteration bootstrap resampling and null-model sensitivity analyses (Robinson-Foulds distance) demonstrated that the interspecies clustering topology of these 26 CpGs is statistically robust and distinct from random genomic noise. These findings suggest partial evolutionary preservation of age-related methylation behavior at human OBS-associated loci, providing a comparative framework for redox-related epigenetic dynamics.
SN  - 1422-0067
ER  -