Articles

Epigenetics and Environmental Health: DNA Methylation Changes Induced by Air Pollution and Cardiovascular Disease

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Cardiovascular disease (CVD) remains the leading global cause of mortality, driven by complex interactions between genetic predisposition and environmental factors, such as ambient air pollution.1 Fine particulate matter (), nitrogen oxides (), and sulfur oxides () are established nontraditional cardiovascular risk factors, triggering both acute events and chronic atherogenesis.3 This systematic review investigates the role of DNA methylation (DNAm)—a primary epigenetic modification—as the molecular transducer linking air pollution exposure to CVD pathology. A systematic search of biomedical databases (PubMed, EMBASE, Web of Science) was conducted to synthesize human observational studies focused on exposure, DNAm changes, and cardiovascular outcomes. The synthesized evidence demonstrates that air pollution induces rapid and systemic epigenetic alterations. Acute exposure to traffic particles (Black Carbon, ) is associated with global hypomethylation of repetitive elements (e.g., LINE-1) within days, suggesting a generalized collapse in cellular methylation capacity.4 Furthermore, gene-specific alterations, such as the hypomethylation of  (Tissue Factor 3) and , drive prothrombotic states and increase the risk of myocardial infarction.5 Mechanistically, inhaled pollutants induce oxidative stress, which disrupts the S-adenosylmethionine () / Sadenosylhomocysteine () ratio, directly inhibiting DNA methyltransferases ().5 These alterations modulate key pathways of atherogenesis, including chronic systemic inflammation (NF- activation) and autonomic nervous system dysfunction (mtDNA D-loop hypomethylation).5 While methodological limitations—primarily heterogeneity in exposure assessment and reliance on peripheral blood cells—persist, the findings confirm that DNA methylation serves as a dynamic biomarker of individual susceptibility and provides compelling molecular targets for future intervention strategies aimed at mitigating the cardiovascular burden of environmental toxins.5

Zinc Metabolism: A Review with Regard to Zn Finger Proteins, DNA Methylation and p53; In Reference to its Deficiency Syndromes and Tracing its Immunological as Well as Epigenetic Relations

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Epigenetics is the branch of biology that studies the effects of environment on genetics and vice versa. It is the connecting link between genotype and phenotype of an individual, and can be widely influenced by the nutrition and availability of certain essential micronutrients, in this review, zinc. Although a trace element, zinc is essential to the body as a core component of more than 300 proteins and enzymes, which when functioning normally impart structural and mechanical capacities to the body tissues and fluids. Zinc is ubiquitous to all parts of the body and regulates various metabolic and biological processes such as cell proliferation, apoptosis, tumorigenesis, along with the regular working of fetal and adult organs. The role of zinc-finger proteins is crucial to impart stability to a protein’s folds and in turn render it functional to play its role in gene expression to serve as oncogenes or tumor suppressor genes. Zinc deficiency is a common occurrence in various parts of the world and is generally due to inadequate intake through the diet but may also manifest itself in an inheritable form. The effects of low zinc on a cellular level can be seen through a diminishing immunity, increased oxidative stress, reduced functionality of the p53 protein leading to tumor formation, incorrect DNA methylation. While phenotypically, zinc deficit can be both congenital and acquired. Some such diseases discussed here are irritable bowel syndrome, acrodermatitis enteropathica, thymic atrophy, celiac disease and preterm birth. In this review, the focus is on the aspect of zinc availability to cells as an epigenetic modulator/regulator and the subsequent consequences arising due to imbalance of zinc in the cell.

Gene Variants and Epigenetics That Lead to Gender Dysphoria

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These days, the rate of gender dysphoria among transgender individuals has increased drastically. Gender dysphoria is a significant issue affecting every aspect of individuals’ daily activities. It induces significant stress and might eventually cause an impairment. Historically, the etiology of gender dysphoria solely focused on the anatomical aspect, mentioning that men’s and women’s brains are distinct. However, it is now believed to be multifactorial, and emerging researchers are trying to shed light on both brain structures and genes that might contribute to gender dysphoria. To explore the possible etiologies of gender dysphoria, this paper reviews the evidence of how epigenetics contributes to gender dysphoria. The basis includes the role of sex-determining genes, anatomical differences among various populations, epigenetics, and mutation of the RYR3 gene. Epigenetics focuses solely on CpGs methylation. Thus far, these mechanisms could not wholly explain the exact mechanism causing gender dysphoria; therefore, additional research is required to disclose this information. Ultimately, understanding the mechanism of gender dysphoria will promote a better quality of life for individuals experiencing gender dysphoria.