Mitochondrial DNA variants and their impact on epigenetic and biological aging in young adulthood
Abstract The pace of biological aging varies between people independently of chronological age and mitochondria dysfunction is a key hallmark of biological aging. We hypothesized that higher functional impact (FI) score of mitochondrial DNA (mtDNA) variants might contribute to premature aging and te...
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| Format: | Article |
| Language: | English |
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Nature Publishing Group
2025-01-01
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| Series: | Translational Psychiatry |
| Online Access: | https://doi.org/10.1038/s41398-025-03235-4 |
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| author | Klara Mareckova Ana Paula Mendes-Silva Martin Jáni Anna Pacinkova Pavel Piler Vanessa F. Gonçalves Yuliya S. Nikolova |
| author_facet | Klara Mareckova Ana Paula Mendes-Silva Martin Jáni Anna Pacinkova Pavel Piler Vanessa F. Gonçalves Yuliya S. Nikolova |
| author_sort | Klara Mareckova |
| collection | DOAJ |
| description | Abstract The pace of biological aging varies between people independently of chronological age and mitochondria dysfunction is a key hallmark of biological aging. We hypothesized that higher functional impact (FI) score of mitochondrial DNA (mtDNA) variants might contribute to premature aging and tested the relationships between a novel FI score of mtDNA variants and epigenetic and biological aging in young adulthood. A total of 81 participants from the European Longitudinal Study of Pregnancy and Childhood (ELSPAC) prenatal birth cohort had good quality genetic data as well as blood-based markers to estimate biological aging in the late 20. A subset of these participants (n = 69) also had epigenetic data to estimate epigenetic aging in the early 20s using Horvath’s epigenetic clock. The novel FI score was calculated based on 7 potentially pathogenic mtDNA variants. Greater FI score of mtDNA variants was associated with older epigenetic age in the early 20s and older biological age in the late 20s. These medium to large effects were independent of sex, current BMI, cigarette smoking, cannabis, and alcohol use. These findings suggest that elevated FI score of mtDNA variants might contribute to premature aging in young adulthood. |
| format | Article |
| id | doaj-art-33fb5e7a46694acc8960b2df977f0162 |
| institution | Kabale University |
| issn | 2158-3188 |
| language | English |
| publishDate | 2025-01-01 |
| publisher | Nature Publishing Group |
| record_format | Article |
| series | Translational Psychiatry |
| spelling | doaj-art-33fb5e7a46694acc8960b2df977f01622025-01-26T12:53:44ZengNature Publishing GroupTranslational Psychiatry2158-31882025-01-011511810.1038/s41398-025-03235-4Mitochondrial DNA variants and their impact on epigenetic and biological aging in young adulthoodKlara Mareckova0Ana Paula Mendes-Silva1Martin Jáni2Anna Pacinkova3Pavel Piler4Vanessa F. Gonçalves5Yuliya S. Nikolova6Brain and Mind Research, Central European Institute of Technology, Masaryk University (CEITEC)Campbell Family Mental Health Research Institute, Centre for Addiction and Mental HealthBrain and Mind Research, Central European Institute of Technology, Masaryk University (CEITEC)Brain and Mind Research, Central European Institute of Technology, Masaryk University (CEITEC)RECETOX Faculty of Science, Masaryk UniveristyCampbell Family Mental Health Research Institute, Centre for Addiction and Mental HealthCampbell Family Mental Health Research Institute, Centre for Addiction and Mental HealthAbstract The pace of biological aging varies between people independently of chronological age and mitochondria dysfunction is a key hallmark of biological aging. We hypothesized that higher functional impact (FI) score of mitochondrial DNA (mtDNA) variants might contribute to premature aging and tested the relationships between a novel FI score of mtDNA variants and epigenetic and biological aging in young adulthood. A total of 81 participants from the European Longitudinal Study of Pregnancy and Childhood (ELSPAC) prenatal birth cohort had good quality genetic data as well as blood-based markers to estimate biological aging in the late 20. A subset of these participants (n = 69) also had epigenetic data to estimate epigenetic aging in the early 20s using Horvath’s epigenetic clock. The novel FI score was calculated based on 7 potentially pathogenic mtDNA variants. Greater FI score of mtDNA variants was associated with older epigenetic age in the early 20s and older biological age in the late 20s. These medium to large effects were independent of sex, current BMI, cigarette smoking, cannabis, and alcohol use. These findings suggest that elevated FI score of mtDNA variants might contribute to premature aging in young adulthood.https://doi.org/10.1038/s41398-025-03235-4 |
| spellingShingle | Klara Mareckova Ana Paula Mendes-Silva Martin Jáni Anna Pacinkova Pavel Piler Vanessa F. Gonçalves Yuliya S. Nikolova Mitochondrial DNA variants and their impact on epigenetic and biological aging in young adulthood Translational Psychiatry |
| title | Mitochondrial DNA variants and their impact on epigenetic and biological aging in young adulthood |
| title_full | Mitochondrial DNA variants and their impact on epigenetic and biological aging in young adulthood |
| title_fullStr | Mitochondrial DNA variants and their impact on epigenetic and biological aging in young adulthood |
| title_full_unstemmed | Mitochondrial DNA variants and their impact on epigenetic and biological aging in young adulthood |
| title_short | Mitochondrial DNA variants and their impact on epigenetic and biological aging in young adulthood |
| title_sort | mitochondrial dna variants and their impact on epigenetic and biological aging in young adulthood |
| url | https://doi.org/10.1038/s41398-025-03235-4 |
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