Cited by 55Epigenetics and DNA MethylationGenetics, Aging, and Longevity in Model OrganismsTelomeres, Telomerase, and Senescence

Synchrony and asynchrony between an epigenetic clock and developmental timing

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Hoshino, Akina, Horvath, Steve, Sridhar, Akshayalakshmi, Chitsazan, Alex, Reh, Thomas A.·2019·Scientific Reports

Abstract

Epigenetic changes have been used to estimate chronological age across the lifespan, and some studies suggest that epigenetic “aging” clocks may already operate in developing tissue. To better understand the relationship between developmental stage and epigenetic age, we utilized the highly regular sequence of development found in the mammalian neural retina and a well-established epigenetic aging clock based on DNA methylation. Our results demonstrate that the epigenetic age of fetal retina is highly correlated with chronological age. We further establish that epigenetic aging progresses normally in vitro, suggesting that epigenetic aging is a property of individual tissues. This correlation is also retained in stem cell-derived retinal organoids, but is accelerated in individuals with Down syndrome, a progeroid-like condition. Overall, our results suggest that epigenetic aging begins as early as a few weeks post-conception, in fetal tissues, and the mechanisms underlying the phenomenon of epigenetic aging might be studied in developing organs.

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  • DNA methylation age estimates of neurons tend to be lower than chronological age but remain correlated, in agreement with previous studies.

    “In agreement with previous studies57,63,64, DNAm age estimates of neurons tend to be lower than their chronological age but remain correlated.”

    From Reprogramming to recover youthful epigenetic information and restore vision (2020) · cites this paper as [64]

    The Epigenetic clock analysis section (page unavailable) says DNAm age correlates with chronological age in sorted neurons. It does not say neuronal DNAm age estimates tend to be lower than chronological age; the paper’s own reported correlation concerns fetal retinal tissue, not isolated neurons. (LLM, conf=0.86)

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Cited by

Sorted by citations

Authors
Hoshino, A., Horvath, S., Sridhar, A., Chitsazan, A., & Reh, T. A.
Affiliations
  • University of Washington (US)
  • University of California, Los Angeles (US)
Corresponding author
Reh, Thomas A.
Venue
Scientific Reports
Published
2019-03-06
Volume
9
Issue
1
Pages
3770-3770
ISSN
2045-2322 (ISSN-L)
OpenAlex
W2919418800
Cited by
55
References
4
Citations by year
2025: 6 · 2024: 7 · 2023: 5 · 2022: 7 · 2021: 11 · 2020: 14 · 2019: 5
FWCI
3.06
Type
journal article
Language
en
Open access
Locations
  • Scientific Reports (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, other-oa)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
Funders
  • Fred Hutchinson Cancer Research Center
  • University of Washington
  • National Institutes of Health
  • National Institute on Aging (U01AG060908)
  • National Eye Institute (P30 EY01730, F32EY025117, R01EY021482, P30EY001730)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
  • Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
Keywords
epigenetic aging, DNA methylation, epigenetic clocks, developmental timing, fetal retina, neural retina development, retinal organoids, Down syndrome, tissue-specific aging, chronological age
MeSH terms
Cells, Cultured, Humans, Organoids, Retina, Cellular Senescence, Sequence Analysis, RNA, CpG Islands, DNA Methylation, Epigenesis, Genetic

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