Exercise-Induced Epigenetic Modifications: Implications for Healthy Aging.

Update on epigenetics in allergic disease

Regulatory T cells (Tregs) are central mediators of immune tolerance, yet within tumors they adopt specialized phenotypes that confer the potent suppression of anti-tumor immune responses. Emerging evidence indicates that this functional plasticity is not driven by genetic alterations but instead arises from dynamic and context-dependent epigenetic reprogramming. While individual epigenetic mechanisms controlling Treg development and stability have been described, how tumor-derived cues reshape Treg epigenetic states, how these programs differ across cancer types, and which features distinguish tumor-infiltrating Tregs from their peripheral counterparts remain incompletely understood. In this review, we synthesize recent advances in DNA methylation, histone modifications, chromatin accessibility, and non-coding RNA regulation that govern Treg identity and function with a particular emphasis on tumor-specific epigenetic adaptations. We highlight emerging epigenetic hallmarks of intratumoral Tregs, discuss unresolved mechanistic questions, and evaluate the therapeutic potential and limitations of targeting epigenetic pathways to selectively modulate Tregs in cancer. By integrating mechanistic, cancer-specific, and translational perspectives, this review aims to provide a conceptual framework for understanding how epigenetic regulation shapes Treg behavior in the tumor microenvironment and how it may be exploited for cancer immunotherapy.

Ovarian cancer (OC) is one of the most lethal gynecologic malignancies globally. In spite of positive responses to initial therapy, the overall survival rates of OC patients remain poor due to the development of drug resistance and consequent cancer recurrence. Indeed, intensive studies have been conducted to unravel the molecular mechanisms underlying OC therapeutic resistance. Besides, emerging evidence suggests a crucial role for epigenetic modifications, namely, DNA methylation, histone modifications, and non-coding RNA regulation, in the drug resistance of OC. These epigenetic modifications contribute to chemoresistance through various mechanisms, namely, upregulating the expression of multidrug resistance proteins (MRPs), remodeling of the tumor microenvironment, and deregulated immune response. Therefore, an in-depth understanding of the role of epigenetic mechanisms in clinical therapeutic resistance may improve the outcome of OC patients. In this review, we will discuss the epigenetic regulation of OC drug resistance and propose the potential clinical implications of epigenetic therapies to prevent or reverse OC drug resistance, which may inspire novel treatment options by targeting resistance mechanisms for drug-resistant OC patients.

Background: Substance use disorder (SUD) is closely associated with epigenetic modifications that significantly impact mental health outcomes. Alcohol and drug misuse induce widespread changes in the epigenome and transcriptome of the central nervous system, disrupting critical processes such as reward signaling and emotional regulation. These alterations in epigenetic regulation and gene expression often persist even after substance cessation, potentially contributing to the onset or worsening of psychiatric conditions, including schizophrenia, depression, stress, and anxiety. Summary: This review delves into key epigenetic mechanisms underlying SUD and its comorbid psychiatric disorders, with a focus on DNA methylation, histone modifications, and noncoding RNA regulation. Additionally, it examines the influence of environmental and biological factors on the epigenome and evaluates emerging epigenetic-based therapeutic strategies aimed at treating SUD and related psychiatric conditions. Key Messages: Gaining a deeper understanding of the epigenetic mechanisms driving SUD and its associated psychiatric disorders is crucial for the development of effective therapeutic interventions. This review highlights the potential of epigenetic-based pharmacological strategies to mitigate the societal and personal burdens linked to SUD and its mental health complications.

Exploring the impact of environmental factors on male reproductive health through epigenetics.

Changes in the epigenome induced by the environment have been documented in diverse animal phyla, ranging from insects to rodents to humans.These include chromatin remodeling, histone tail modifi cations, and DNA methylation, and more recently the list has expanded to encompass noncoding RNA and microRNA gene regulation (Matzke and Birchler 2005).Thus, it is increasingly recognized that exposure to chemical, nutritional, behavioral, and physical factors alters gene expression and affects health and disease not only through mutation of but also through modifi cation of the epigenome.Moreover, such exposures have been directly linked with subsequent disease formation through deregulation of epigenetic mechanisms.Unlike genetic mutations, these epigenetic changes are potentially reversible, providing a unique avenue to improve human health.Consequently research in epigenetics has increased dramatically in the last few years (Figure 1).The term "epigenetics" was popularized in the early 1940s by developmental biologist Conrad Waddington (1940) to explain "the interactions of genes with their environment, which bring the phenotype into being."In the 1970s, Holliday and Pugh (1975) fi rst proposed covalent chemical DNA modifi cations, including methylation of cytosine-guanine (CpG) dinucleotides, as the molecular mechanism to explain Waddington's hypothesis.The revelations several decades later that X inactivation in mammals and genomic imprinting are regulated by complex and multifactorial mechanisms (Monk 1988;Willard et al. 1993) resulted in an updated definition, describing epigenetics as heritable changes in gene expression that occur without a change in DNA sequence, including the modifi cation of DNA methylation and chromatin remodeling (Wolfe and Matzke 1999).The genomics revolution inspired the investigation of genome-wide rather than local gene analyses, and the term "epigenomics" was

Epigenetic regulation of cellular identity and function is at least partly achieved through changes in covalent modifications on DNA and histones. Much progress has been made in recent years to understand how these covalent modifications affect cell identity and function. Despite the advances, whether and how epigenetic factors contribute to memory formation is still poorly understood. In this review, we discuss recent progress in elucidating epigenetic mechanisms of learning and memory, primarily at the DNA level, and look ahead to discuss their potential implications in reward memory and development of drug addiction.

Epigenetics refers to genetic regulation patterns that gene expressions, which lead to the phenotype variance, are modified in the absence of changes of DNA sequence. Epigenetics mainly includes DNA methylation, histone modification, and non-coding RNA regulation. During the development of the teeth, conventional gene regulation and epigenetics synergistically regulate the spatial and temporal expression of genes, which involved in cell proliferation, differentiation and finally the formation of teeth. Exploration of the epigenetic regulation mechanisms during tooth development can provide multiple clues and ideas for the research of tooth regeneration. This article reviewed the significant roles of epigenetic regulation in tooth development.

Nutrigenomics explore how foods and bioactive compounds interact with our genes and epigenome to influence overall health, while food safety examines how dietary hazards can disrupt these pathways. Integrating both fields aids in the prevention and management of chronic non-communicable diseases (NCDs). Nutrients such as polyphenols, omega-3 fatty acids and methyl donors can modulate key epigenetic mechanisms, including DNA methylation, histone modifications and non-coding RNA regulation, helping protect against metabolic disorders and some types of cancer. Conversely, exposure to harmful substances, including mycotoxins, heavy metals, endocrine-disrupting chemicals and food processing by-products, can trigger oxidative stress, disturb the gut microbiome and alter epigenetic regulation, increasing disease risk. This narrative, non-systematic review synthesizes evidence published between 2000 and 2025, emphasizing the surge in studies since 2020. Relevant articles were retrieved from PubMed, Scopus, Web of Science and Google Scholar using combinations of keywords related to nutrigenomics, epigenetics, food safety, and chronic diseases. In total, 235 publications were analyzed, highlighting nutrigenomics and food safety as an emerging scientific hotspot. Recent advances in multi-omics and microbiome research have enabled precision nutrition approaches and more accurate risk assessment models for NCDs. Despite challenges such as inconsistent methodologies and limited longitudinal data, integrating nutrigenomics with food safety offers a promising approach for improving metabolic health, achieving sustainable weight management, and reducing the global burden of chronic disease. Priorities include large-scale clinical trials, standardized omics pipelines and validated biomarkers to ensure accessibility to and translational impact in public health.

Metastatic dissemination of epithelial ovarian cancer (EOC) predominantly occurs through direct cell shedding from the primary tumor into the intra-abdominal cavity that is filled with malignant ascitic effusions. Facilitated by the fluid flow, cells distribute throughout the cavity, broadly seed and invade through peritoneal lining, and resume secondary tumor growth in abdominal and pelvic organs. At all steps of this unique metastatic process, cancer cells exist within a multidimensional tumor microenvironment consisting of intraperitoneally residing cancer-reprogramed fibroblasts, adipose, immune, mesenchymal stem, mesothelial, and vascular cells that exert miscellaneous bioactive molecules into malignant ascites and contribute to EOC progression and metastasis via distinct molecular mechanisms and epigenetic dysregulation. This review outlines basic epigenetic mechanisms, including DNA methylation, histone modifications, chromatin remodeling, and non-coding RNA regulators, and summarizes current knowledge on reciprocal interactions between each participant of the EOC cellular milieu and tumor cells in the context of aberrant epigenetic crosstalk. Promising research directions and potential therapeutic strategies that may encompass epigenetic tailoring as a component of complex EOC treatment are discussed.

Globally, arboviral infections are major public health threats, and diseases caused by arboviruses-mainly Zika virus, Dengue virus, West Nile virus, and Japanese encephalitis virus-affect many people. Arboviruses can induce severe neurological disorders through complex interactions with host cellular and immune pathways. Recent global surges in infections highlight the urgent need to understand their neuropathogenic mechanisms. Increasing evidence shows that arboviruses exploit host epigenetic machinery, including DNA methylation, histone modification, and non-coding RNA regulation, to subvert antiviral defenses, modulate immune responses, and promote viral infection within the central nervous system. Here, we summarise current findings on the epigenetic regulation of arboviral infections and their contribution to neuropathology. We also discuss how the reversibility of epigenetic modifications presents novel therapeutic opportunities, with inhibitors targeting histone deacetylases, methyltransferases, and DNA methyltransferases emerging as potential antiviral interventions. Advances in epigenomic profiling offer unprecedented opportunities to dissect virus-host interactions, providing a foundation for precision therapies aimed at mitigating arboviral neuroinvasion and its long-term neurological consequences.

Molecular mechanisms associated with inflammation-promoted tumorigenesis have become an important topic in cancer research. Various abnormal epigenetic changes, including DNA methylation, histone modification, chromatin remodeling, and noncoding RNA regulation, occur during the transformation of chronic inflammation into colorectal cancer (CRC). These changes not only accelerate transformation but also lead to cancer progression and metastasis by activating carcinogenic signaling pathways. The NF-κB and STAT3 signaling pathways play a particularly important role in the transformation of inflammation into CRC, and both are critical to cellular signal transduction and constantly activated in cancer by various abnormal changes including epigenetics. The NF-κB and STAT3 signals contribute to the microenvironment for tumorigenesis through secretion of a large number of pro-inflammatory cytokines and their crosstalk in the nucleus makes it even more difficult to treat CRC. Compared with gene mutation that is irreversible, epigenetic inheritance is reversible or can be altered by the intervention. Therefore, understanding the role of epigenetic inheritance in the inflammation-cancer transformation may elucidate the pathogenesis of CRC and promote the development of innovative drugs targeting transformation to prevent and treat this malignancy. This review summarizes the literature on the roles of epigenetic mechanisms in the occurrence and development of inflammation-induced CRC. Exploring the role of epigenetics in the transformation of inflammation into CRC may help stimulate futures studies on the role of molecular therapy in CRC.

BackgroundAsthma is a prevalent chronic inflammatory disease, and recent research highlights the role of epigenetic modifications, such as DNA and RNA methylation, in its pathogenesis. This study aims to provide a comprehensive bibliometric analysis to evaluate research trends and hotspots in DNA and RNA methylation within asthma-related research.ResultsData were extracted from the Web of Science Core Collection, focusing on English-language publications. Bibliometric tools, including VOSviewer and CiteSpace, were used to analyze publication metrics, author contributions, and keyword trends. The analysis revealed that DNA methylation research in asthma began in 1994 and has shown significant annual growth, while RNA methylation research started a year earlier but with a slightly slower growth trajectory. The United States, China, and the United Kingdom are the leading contributors, with Harvard University being notably influential. Research on DNA methylation has shown higher rates of international collaboration. Despite substantial growth in both areas, recent years have seen a decline in annual publications and citations. The "Journal of Allergy and Clinical Immunology" was identified as the most influential journal in this field. While DNA methylation research is more mature, RNA methylation is gaining prominence, particularly in understanding asthma pathogenesis. Future research should focus on underdeveloped areas, such as "sublingual immunotherapy" and "occupational asthma" for DNA methylation, and "obesity", "lncRNA", "miRNA", "vitamin D", and methylation markers such as "m6A", "m5C", and "m7G" for RNA methylation.ConclusionsThis bibliometric analysis provides a detailed overview of the research landscape in DNA and RNA methylation in asthma. The findings highlight significant growth and collaboration in this field, with specific areas identified for future research. Understanding these trends can help guide future studies and potentially lead to new therapeutic approaches for asthma.

Epigenetic flexibility in metabolic regulation: disease cause and prevention?

DNA methylation plays crucial roles in many biological processes and abnormal DNA methylation patterns are often observed in diseases. Recent studies have shed light on cis-acting DNA elements that regulate locus-specific DNA methylation, which involves transcription factors, histone modification and DNA secondary structures. In addition, several recent studies have surveyed DNA motifs that regulate DNA methylation and suggest potential applications in diagnosis and prognosis. Here, we discuss the current biological foundation for the cis-acting genetic code that regulates DNA methylation. We review the computational models that predict DNA methylation with genetic features and discuss the biological insights revealed from these models. We also provide an in-depth discussion on how to leverage such knowledge in clinical applications, particularly in the context of liquid biopsy for early cancer diagnosis and treatment.