Journal of Clinical Epigenetics Open Access

  • ISSN: 2472-1158
  • Journal h-index: 10
  • Average acceptance to publication time (5-7 days)
  • Average article processing time (30-45 days) Less than 5 volumes 30 days
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Commentary - (2022) Volume 8, Issue 5

Modifications Used in DNA Methylation of Aging Epigenetics
Mary Ashun*
 
Department of Clinical Epigenetics, University of Princeton, USA
 
*Correspondence: Mary Ashun, Department of Clinical Epigenetics, University of Princeton, USA, Email:

Received: 04-May-2022, Manuscript No. IPJCE-22-13477; Editor assigned: 06-May-2022, Pre QC No. IPJCE-22-13477 (PQ); Reviewed: 20-May-2022, QC No. IPJCE-22-13477; Revised: 24-May-2022, Manuscript No. IPJCE-22-13477 (R); Published: 01-Jun-2022, DOI: 10.21767/2472-1158-22.8.21

Description

Brain development is a lifelong process that involves several important transitional periods in which significant cognitive changes occur. Embryo development, puberty, and reproductive aging are transitional periods that are sensitive to environmental factors. Rather than isolated episodes, each transition is built on the last episode and is subject to subsequent changes that occur in previous transitions. Epigenetic marks such as DNA methylation and histone modifications provide a mechanism by which early events affect developmental, cognitive, and health outcomes.

Cellular senescence is a heterogeneous process controlled by the genetic, epigenetic, and environmental factors that characterize many types of somatic cells. It has been suggested as a sign of aging that contributes to aging and chronic illness. Senescent cells (SCs) exhibit a specific senescence-related secretory phenotype (SASP) that is primarily characterized by the production of pro-inflammatory and matrix-degrading molecules. Accumulation of SC induces a chronic, mild, systemic inflammation known as inflammation. This chronic activation of the immune system leads to a decrease in SC clearance, leading to a vicious circle that promotes inflammation. Accumulation of SC is a factor that causes various age-related medical conditions.

Aging is associated with progressive and dysfunction of all tissues and a marked increase in many “age diseases”. Aging has long been regarded as an unavoidable process, but recently strategies have been developed to delay and in some cases reverse the aging process. Here we review a new rejuvenation strategy based on reprogramming for versatility. Some of these approaches can ultimately lead to medicinal properties to improve health and longevity.

Given the social and healthy costs of our aging population, operations to delay biological aging and increase health spans are interesting. Here we report a randomized controlled clinical trial of 43 healthy adult males aged 5072. The 8-week treatment program included diet, sleep, exercise, relaxation guidance, and supplemental probiotics and phytonutrients. The control group received no intervention.

Aging has become one of the fastest growing research topics in biology. However, it is unclear how the aging process works exactly. Epigenetics plays an important role, and multiple epigenetic interventions can regulate lifespan. This white paper describes the interaction between epigenetics and aging and how to use epigenetic reprogramming to reverse age. Partial in vivo reprogramming holds great promise as a potential treatment, but some limitations remain. Rejuvenation by reprogramming is a young but rapidly expanding subfield in the biology of aging.

Cellular senescence is an essential tumor suppressor mechanism that prevents the growth of carcinogenically activated, genetically unstable, and/or damaged cells. Inducing aging of tumor cells is also one of the fundamental mechanisms by which cancer treatment exerts antitumor activity. However, the accumulation of evidence from preclinical trials indicates that radiation therapy and chemotherapy cause the accumulation of senescent cells (SnC) in both tumor and normal tissue. Paradoxically, SnC in tumors can promote tumor recurrence, metastasis, and resistance to treatment, partly through the expression of aging-related secretory phenotypes.

Conclusion

One of the main features of aging is the progressive loss of physiological integrity, which weakens physical function and increases the risk of death. Robust biomarkers are important for estimating a person’s biological age, aging rate, and health status. A new biomarker of aging, the DNA methylation clock consists of a panel of guanine dinucleotides of cytosine phosphate, which can be used to accurately measure subjective age. These clocks are considered chronologically accurate biomarkers for humans and other vertebrates. Many studies have shown that these watches quantify the rate of biological aging and the effects of longevity and anti-aging interventions. This review describes the purpose and use of DNA methylation clocks in aging research.

Acknowledgement

None.

Conflict of Interest

The author declares there is no conflict of interest in publishing this article.

Citation: Ashun M (2022) Modifications Used in DNA Methylation of Aging Epigenetics J Clin Epigen.8:21.

Copyright: © Ashun M. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited