Health outcomes in SARS survivors 18 years after infection: A longitudinal cohort study
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA893211 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR22013500_1.fastq.gz | Fastqsanger.gz | |||
| SRR22013500_2.fastq.gz | Fastqsanger.gz | |||
| SRR22013501_1.fastq.gz | Fastqsanger.gz | |||
| SRR22013501_2.fastq.gz | Fastqsanger.gz | |||
| SRR22013502_1.fastq.gz | Fastqsanger.gz |
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Project description:Long-term survivors of childhood cancer experience treatment-related cardiotoxicity among a broad spectrum of chronic health conditions, which may be further aggrevated by suboptimal life-course social/behavioral/environmental exposures. Epigenetic mechanisms, particularly DNA methylation (DNAm), provide a potential link through which these exposures become biologically embedded and subsequently influence long-term health outcomes. Epigenome-wide association studies (EWAS) identified DNAm signatures associated with both treatment effects as well as life-course exposures. In parallel, DNAm variations were also evaluated in relation to cardiometabolic risk factors, cardiovascular diseases, and other chronic health conditions, revealing individual CpG sites or genes/geomic regions where these CpGs reside linked to clinically relevant phenotypes. Together, these findings support DNAm as a molecular interface connecting diverse exposures to adverse health outcomes. In addition, epigenetic age acceleration, assessed using DNAm-based aging biomarkers, was observed among survivors exposed to cancer treatments. Epigenetic age acceleration mediated a substantial proportion of the associations between cancer treatment exposures and cardiometabolic risk factors or cardiovascular diseases, supporting accelerated biological aging as a key pathway linking cancer treatment to long-term morbidity. Lifestyle and health behaviors, as well as social vulnerability and psychosocial stress, were also associated with variations in epigenetic age acceleration, highlighting the potential modifiability of aging-related pathways in ameliorating late-effects among childhood cancer survivors. In conclusion, these findings establish DNAm—captured through EWAS signatures and epigenetic age acceleration—as central molecular mechanisms linking treatment effects and life-course exposures to cardiotoxicity along with other chronic health conditions in childhood cancer survivors. This integrative epigenetic framework supports the use of DNAm-based biomarkers for risk stratification and nominates modifiable pathways as potential intervention targets to improve long-term survivorship outcomes.
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Project description:Background: Early life epigenetic programming influences adult health outcomes. Moreover, DNA methylation levels have been found to change more rapidly during the first years of life. Our aim was the identification and characterization of the CpG sites that are modified with time during the first years of life. We hypothesize that these DNA methylation changes would lead to the detection of genes that might be epigenetically modulated by environmental factors during early childhood and which, if disturbed, might contribute to susceptibility to diseases later in life. Methods: The study of the DNA methylation pattern of 485577 CpG sites was performed on 30 blood samples from 15 subjects, collected both at birth and at 5 years old, using Illumina® Infinium 450 k array. To identify differentially methylated CpG (dmCpG) sites, the methylation status of each probe was examined using linear models and the Empirical Bayes Moderated t test implemented in the limma package of R/Bioconductor. Surogate variable analysis was used to account for batch effects. Results: DNA methylation levels significantly changed from birth to 5 years of age in 6641 CpG sites. Of these, 36.79 % were hypermethylated and were associated with genes related mainly to developmental ontology terms, while 63.21 % were hypomethylated probes and associated with genes related to immune function. Conclusions: Our results suggest that DNA methylation alterations with age during the first years of life might play a significant role in development and the regulation of leukocyte-specific functions. This supports the idea that blood leukocytes experience genome remodeling related to their interaction with environmental factors, underlining the importance of environmental exposures during the first years of life and suggesting that new strategies should be take into consideration for disease prevention. Longitudinal study including 15 samples
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Project description:Extensive epigenetic remodelling takes place during early life; however, the alterations of DNA methylation that occur during this period have not been sufficiently addressed by longitudinal studies. We made use of the most recent Illumina MethylationEPIC Beadchip platform to characterize genome-wide DNA methylation changes observed through the first 10 years of life in longitudinal blood samples of 11 subjects. We described numerous changes during the first 5 years, while many less alterations in the following 5 year period. Interestingly, we identified a subset of persistent DNA methylation changes of considerable magnitude along the first 10 years of life. Moreover, our data demonstrated that genes that suffer simultaneous hyper- and hypomethylation are functionally different from genes that are exclusively hyper- or hypomethylated. Furthermore, our results evidence that enhancer-associated methylation changes are different for the gain or loss of methylation. throughout hematopoietic maturation by analyzing multiple hematopoietic cell types at different developmental stages. We identified a plethora of DNA methylation changes that occur during human hematopoietic differentiation. Interestingly, we observed that T lymphocytes display a substantial enhancement of de novo CpG hypermethylation as compared to other hematopoietic cell populations.
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