DNA Methylation Biomarkers in Aging and Age-Related Diseases

Salameh, Yasmeen; Bejaoui, Yosra; Hajj, Nady El

doi:10.3389/fgene.2020.00171

Cited by 173 publications

(126 citation statements)

References 136 publications

(139 reference statements)

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“…These differences have been interpreted to reflect different speeds of biological aging, and can even be used to predict all-cause mortality 26 . Furthermore, many pathological conditions are associated with epigenetic age acceleration in humans, while anti-aging diets in mice have been shown to result in age deceleration 24 , 27 . The available findings in humans and mice thus suggest that differences between methylation age and chronological age can be used as health biomarkers, with age acceleration indicating poor health and age deceleration indicating good health.…”

Section: Introductionmentioning

confidence: 99%

A chicken DNA methylation clock for the prediction of broiler health

et al. 2021

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The domestic chicken (Gallus gallus domesticus) is the globally most important source of commercially produced meat. While genetic approaches have played an important role in the development of chicken stocks, little is known about chicken epigenetics. We have systematically analyzed the chicken DNA methylation machinery and DNA methylation landscape. While overall DNA methylation distribution was similar to mammals, sperm DNA appeared hypomethylated, which correlates with the absence of the DNMT3L cofactor in the chicken genome. Additional analysis revealed the presence of low-methylated regions, which are conserved gene regulatory elements that show tissue-specific methylation patterns. We also used whole-genome bisulfite sequencing to generate 56 single-base resolution methylomes from various tissues and developmental time points to establish an LMR-based DNA methylation clock for broiler chicken age prediction. This clock was used to demonstrate epigenetic age acceleration in animals with experimentally induced inflammation. Our study provides detailed insights into the chicken methylome and suggests a novel application of the DNA methylation clock as a marker for livestock health.

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Section: Introductionmentioning

confidence: 99%

A chicken DNA methylation clock for the prediction of broiler health

et al. 2021

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“…Data now show it is possible to determine someone’s epigenetic age and compare it with their chronological age. There is a close correlation with this ratio and co-existing morbidity [ 287 ]. Thus, would blood-derived epigenetic markers of metabolic age correlate with disease severity before, during and after infection?…”

Section: Can We Test the Hypothesis That Mitochondrial Health = Immunmentioning

confidence: 99%

SARS-CoV-2 and mitochondrial health: implications of lifestyle and ageing

Nunn

Guy²,

Brysch

et al. 2020

Immun Ageing

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Infection with SARs-COV-2 displays increasing fatality with age and underlying co-morbidity, in particular, with markers of the metabolic syndrome and diabetes, which seems to be associated with a “cytokine storm” and an altered immune response. This suggests that a key contributory factor could be immunosenescence that is both age-related and lifestyle-induced. As the immune system itself is heavily reliant on mitochondrial function, then maintaining a healthy mitochondrial system may play a key role in resisting the virus, both directly, and indirectly by ensuring a good vaccine response. Furthermore, as viruses in general, and quite possibly this new virus, have also evolved to modulate immunometabolism and thus mitochondrial function to ensure their replication, this could further stress cellular bioenergetics. Unlike most sedentary modern humans, one of the natural hosts for the virus, the bat, has to “exercise” regularly to find food, which continually provides a powerful adaptive stimulus to maintain functional muscle and mitochondria. In effect the bat is exposed to regular hormetic stimuli, which could provide clues on how to resist this virus. In this paper we review the data that might support the idea that mitochondrial health, induced by a healthy lifestyle, could be a key factor in resisting the virus, and for those people who are perhaps not in optimal health, treatments that could support mitochondrial function might be pivotal to their long-term recovery.

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“… 6 , 143 This can be explained by the upregulation of ACE2 expression by Estrogen, 4 , 131 and the X-chromosomal location of the ACE2 gene 3 , 129 , 144 (which is regulated epigenetically via DNA methylation). 12 , 13 DNA methylation is associated with biological age, 12 , 145 , 146 which suggests that biological age may be a more accurate risk factor for severe COVID-19 complications compared to chronological age. 13 , 147 This pattern of ACE2 expression may partly explain why elevated ACE2 levels possibly have no negative effects on COVID-19 susceptibility.…”

Section: Renin Angiotensin Aldosterone Systemmentioning

confidence: 99%

Angiotensin-converting enzyme 2, the complement system, the kallikrein-kinin system, type-2 diabetes, interleukin-6, and their interactions regarding the complex COVID-19 pathophysiological crossroads

Hoevenaar

Goossens

Roorda³

2020

J Renin Angiotensin Aldosterone Syst

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Because of the current COVID-19-pandemic, the world is currently being held hostage in various lockdowns. ACE2 facilitates SARS-CoV-2 cell-entry, and is at the very center of several pathophysiological pathways regarding the RAAS, CS, KKS, T2DM, and IL-6. Their interactions with severe COVID-19 complications (e.g. ARDS and thrombosis), and potential therapeutic targets for pharmacological intervention, will be reviewed.

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DNA Methylation Biomarkers in Aging and Age-Related Diseases

Cited by 173 publications

References 136 publications

A chicken DNA methylation clock for the prediction of broiler health

A chicken DNA methylation clock for the prediction of broiler health

SARS-CoV-2 and mitochondrial health: implications of lifestyle and ageing

Angiotensin-converting enzyme 2, the complement system, the kallikrein-kinin system, type-2 diabetes, interleukin-6, and their interactions regarding the complex COVID-19 pathophysiological crossroads

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