Epigenetic changes during ageing and their underlying mechanisms

Braga, Deisi L.; Mousovich-Neto, Felippe; Tonon-da-Silva, Guilherme; Salgueiro, Willian G.; Mori, Marcelo A.

doi:10.1007/s10522-020-09874-y

Cited by 18 publications

(7 citation statements)

References 227 publications

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“…Epigenetic alterations to nucleic acids are a component of the normal cellular signaling landscape. Alterations to patterns of epigenetic profiles across the aging process are potentially one of the key factors for controlling individual healthy aging trajectories [70][71][72]. As aging is linked with altered epigenetic mechanisms of gene regulation, such as DNA methylation, histone modification and chromatin remodeling, and non-coding RNAs, the potential therapeutic control of these mechanisms is a potentially effective strategy for interdicting the generation of pathological aging phenotypes.…”

Section: Epigenetic Alterationsmentioning

confidence: 99%

The Relaxin-3 Receptor, RXFP3, Is a Modulator of Aging-Related Disease

Leysen

Walter

Clauwaert

et al. 2022

IJMS

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During the aging process our body becomes less well equipped to deal with cellular stress, resulting in an increase in unrepaired damage. This causes varying degrees of impaired functionality and an increased risk of mortality. One of the most effective anti-aging strategies involves interventions that combine simultaneous glucometabolic support with augmented DNA damage protection/repair. Thus, it seems prudent to develop therapeutic strategies that target this combinatorial approach. Studies have shown that the ADP-ribosylation factor (ARF) GTPase activating protein GIT2 (GIT2) acts as a keystone protein in the aging process. GIT2 can control both DNA repair and glucose metabolism. Through in vivo co-regulation analyses it was found that GIT2 forms a close coexpression-based relationship with the relaxin-3 receptor (RXFP3). Cellular RXFP3 expression is directly affected by DNA damage and oxidative stress. Overexpression or stimulation of this receptor, by its endogenous ligand relaxin 3 (RLN3), can regulate the DNA damage response and repair processes. Interestingly, RLN3 is an insulin-like peptide and has been shown to control multiple disease processes linked to aging mechanisms, e.g., anxiety, depression, memory dysfunction, appetite, and anti-apoptotic mechanisms. Here we discuss the molecular mechanisms underlying the various roles of RXFP3/RLN3 signaling in aging and age-related disorders.

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Section: Epigenetic Alterationsmentioning

confidence: 99%

The Relaxin-3 Receptor, RXFP3, Is a Modulator of Aging-Related Disease

Leysen

Walter

Clauwaert

et al. 2022

IJMS

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“…258,262,265 Studies have identified an epigenetic clock that has specific age-related changes in DNA methylation patterns. The epigenetic clock predicts the biological age of an individual that is not necessarily the same as the individual's chronological age 266 and could be a valuable biomarker in predicting adverse health outcomes. 267 For reviews on epigenetic clocks see.…”

Section: Epigenetics and Agingmentioning

confidence: 99%

SARS‐CoV‐2 multifaceted interaction with the human host. Part II: Innate immunity response, immunopathology, and epigenetics

Beacon

Su²,

Lakowski

et al. 2020

IUBMB Life

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The SARS-CoV-2 makes its way into the cell via the ACE2 receptor and the proteolytic action of TMPRSS2. In response to the SARS-CoV-2 infection, the innate immune response is the first line of defense, triggering multiple signaling pathways to produce interferons, pro-inflammatory cytokines and chemokines, and initiating the adaptive immune response against the virus. Unsurprisingly, the virus has developed strategies to evade detection, which can result in delayed, excessive activation of the innate immune system. The response elicited by the host depends on multiple factors, including health status, age, and sex. An overactive innate immune response can lead to a cytokine storm, inflammation, and vascular disruption, leading to the vast array of symptoms exhibited by COVID-19 patients. What is known about the expression and epigenetic regulation of the ACE2 gene and the various players in the host response are explored in this review.

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“…While early life may be the most sensitive period for epigenetic processes, the accumulation of experience over a life course can also alter the epigenome, through potentially environmentally influenced or stochastic changes, as evidenced by identical twins reared apart (20,21) and aging studies (22)(23)(24). When environmentally influenced, epigenetic changes may be a mechanism for the process of weathering, whereby the cumulative effect of social disadvantage over time, such as poverty or discrimination, disproportionately affects the health of disadvantaged populations (25,26).…”

Section: Introductionmentioning

confidence: 99%

Epigenetics as a Mechanism of Developmental Embodiment of Stress, Resilience, and Cardiometabolic Risk Across Generations of Latinx Immigrant Families

Clausing

Non

2021

Front. Psychiatry

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Psychosocial stressors can become embodied to alter biology throughout the life course in ways that may have lasting health consequences. Immigrants are particularly vulnerable to high burdens of stress, which have heightened in the current sociopolitical climate. This study is an investigation of how immigration-related stress (IRS) may impact the cardiometabolic risk and epigenetic markers of Latinx immigrant mothers and children in Nashville, TN. We compared stress and resilience factors reported by Latina immigrant mothers and their children (aged 5–13) from two time points spanning the 2016 U.S. presidential election (June 2015–June 2016 baseline, n = 81; March–September 2018 follow-up, n = 39) with cardiometabolic risk markers (BMI, waist circumference, and blood pressure). We also analyzed these factors in relation to DNA methylation in saliva of stress-related candidate genes (SLC6A4 and FKBP5), generated via bisulfite pyrosequencing (complete case n's range from 67–72 baseline and 29–31 follow-up) (n's range from 80 baseline to 36 follow-up). We found various associations with cardiometabolic risk, such as higher social support and greater acculturation were associated with lower BMI in mothers; discrimination and school stress associated with greater waist circumferences in children. Very few exposures associated with FKBP5, but various stressors associated with methylation at many sites in SLC6A4, including immigrant-related stress in both mothers and children, and fear of parent deportation in children. Additionally, in the mothers, total maternal stress, health stress, and subjective social status associated with methylation at multiple sites of SLC6A4. Acculturation associated with methylation in mothers in both genes, though directions of effect varied over time. We also find DNA methylation at SLC6A4 associates with measures of adiposity and blood pressure, suggesting that methylation may be on the pathway linking stress with cardiometabolic risk. More research is needed to determine the role of these epigenetic differences in contributing to embodiment of stress across generations.

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Epigenetic changes during ageing and their underlying mechanisms

Cited by 18 publications

References 227 publications

The Relaxin-3 Receptor, RXFP3, Is a Modulator of Aging-Related Disease

The Relaxin-3 Receptor, RXFP3, Is a Modulator of Aging-Related Disease

SARS‐CoV‐2 multifaceted interaction with the human host. Part II: Innate immunity response, immunopathology, and epigenetics

Epigenetics as a Mechanism of Developmental Embodiment of Stress, Resilience, and Cardiometabolic Risk Across Generations of Latinx Immigrant Families

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