Environmental Epigenetics最新文献

{"title":"Silent regulators of trauma: the microRNA blueprint underlying post-traumatic stress disorder biology.","authors":"Yogesh Dwivedi, Kevin Prall, Richard C Shelton","doi":"10.1093/eep/dvag024","DOIUrl":"10.1093/eep/dvag024","url":null,"abstract":"<p><p>Post-traumatic stress disorder (PTSD) is a chronic and disabling psychiatric condition that affects millions of people worldwide, producing persistent disturbances in emotional regulation, cognition, and physiological functioning. Although exposure to traumatic or life-threatening events is a defining feature of PTSD, only a subset of exposed individuals develop enduring symptoms, highlighting variability in vulnerability and recovery. The biological mechanisms underlying PTSD remain incompletely understood. Increasing evidence suggests that epigenetic processes play a central role in shaping individual responses to trauma. Among these, microRNAs (miRNAs), small, noncoding RNA molecules that fine-tune gene expression by regulating the translation and stability of multiple target genes simultaneously, have emerged as important epigenetic regulators of PTSD-related neurobiology. Because a single miRNA can influence extensive gene networks, alterations in miRNA expression affect a broad range of biological processes relevant to PTSD, including hypothalamic-pituitary-adrenal (HPA) axis function, synaptic plasticity, immune signaling, and memory formation. Recent studies demonstrate that dysregulated miRNAs can modify glucocorticoid receptor sensitivity, shape fear memory acquisition and extinction, and contribute to the proinflammatory phenotype frequently observed in PTSD. Progress of miRNA research in this field has been driven by integrative strategies that combine human peripheral tissues, plasma, and extracellular vesicles, complemented by animal models of stress and fear learning, including fear conditioning, restraint stress, and single-prolonged stress paradigms. Together, these approaches provide converging evidence for a critical role of miRNAs in PTSD pathophysiology. This review synthesizes findings across species to clarify miRNA-mediated mechanisms and highlight future directions for biomarker discovery and therapeutic development.</p>","PeriodicalId":11774,"journal":{"name":"Environmental Epigenetics","volume":"12 1","pages":"dvag024"},"PeriodicalIF":4.3,"publicationDate":"2026-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13450710/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148697220","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gene-specific DNA methylation responses to Pb²⁺ exposure in aged male zebrafish and associations with locomotor dysfunction.","authors":"Chia-Chen Wu, Danielle N Meyer, Grace A Winny, Dayita Banerjee, Tracie R Baker","doi":"10.1093/eep/dvag023","DOIUrl":"10.1093/eep/dvag023","url":null,"abstract":"<p><p>Lead (Pb²⁺) is a well-established neurotoxin that impairs motor, learning, and memory functions, particularly in children and younger adults. However, its impact on older adults remains less understood. Pb²⁺ toxicity involves disruption of DNA methyltransferase activity and associated epigenetic pathways, potentially altering the expression of specific genes relevant to neurological functions. As methylation patterns naturally shift during aging, Pb²⁺ exposure may induce additional neurological risks in aged populations. Using a zebrafish model, we investigated the combined effects of Pb²⁺ exposure and brain aging. Two-year-old male zebrafish were exposed to 1, 10, 100, 1000, 10 000 µg/l Pb²⁺ or fish water control for five days. Brain tissues were collected for DNA extraction and whole-genome bisulfite sequencing to assess global and gene-specific methylation changes. Our results found that Pb²⁺ exposures ≥ 100 μg/l significantly increased global methylation levels in the aged brain. Differentially methylated genes (DMGs) exhibited methylation changes within gene body regions and were mostly annotated with ion transportation and signal transduction pathways. Although only a limited number of DMGs showed corresponding changes in gene expression, several of them were associated with locomotor-related functions, including <i>shank1</i> at 10 000 Pb²⁺ μg/l, and <i>ptprsa, plxna2</i>, and <i>aopep</i> at 100 μg/l Pb²⁺. These findings suggest that Pb²⁺ exposure during aging predominantly induces gene body-localized DNA methylation changes, and the role of such epigenetic regulation in Pb-associated neurobehavioral outcomes warrants further investigation.</p>","PeriodicalId":11774,"journal":{"name":"Environmental Epigenetics","volume":"12 1","pages":"dvag023"},"PeriodicalIF":4.3,"publicationDate":"2026-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13411783/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148618976","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of RNAi-by-feeding on DNA methyltransferases in <i>Daphnia pulex</i>.","authors":"Trenton C Agrelius, Krista Harmon, Allison Reed, Samuel B Burnett, Rekha C Patel, Jeffry L Dudycha","doi":"10.1093/eep/dvag022","DOIUrl":"10.1093/eep/dvag022","url":null,"abstract":"<p><p>DNA methyltransferases (DNMTs) are well-characterized epigenetic enzymes responsible for transferring methyl groups to and from DNA. Three main DNMT orthologues differ in function and methylation capability. They each are evolutionarily conserved across diverse taxa, but few studies investigate them jointly. We did so in <i>Daphnia</i>, freshwater microcrustaceans used extensively in research on genetic diversity, phenotypic plasticity, and maternal effects. <i>Daphnia</i> are capable of reproducing asexually through cyclic parthenogenesis, making the <i>Daphnia</i> system an ideal choice for studying epigenetic phenomena. Advances in gene expression control techniques, including RNA interference (RNAi), have increased the versatility and power of the <i>Daphnia</i> system. RNAi is a post-transcriptional gene silencing mechanism that operates through sequence-specific cleavage of endogenous messenger RNA transcripts. Here, we used an RNAi bacterial feeding regime to target the three DNMT genes in two clones of <i>Daphnia pulex</i>. We observed significant genotypic differences in response to the RNAi feeding regime, namely, the mortality of one clone. In the other, DNMT expression significantly increased in five of the six experimental treatments, with the highest level observed in animals treated with the GFP double-stranded RNA bacterial vector control. However, DNMT expression was reduced in all three DNMT RNAi treatments relative to the GFP control. Furthermore, we found strong cross-reactivity, where targeting one DNMT resulted in a reduction in expression of the other two. This response may be associated with known immune pathways involving signal transduction that can be stimulated by viral and bacterial signals, or it may result from previously unknown aspects of DNMT biology.</p>","PeriodicalId":11774,"journal":{"name":"Environmental Epigenetics","volume":"12 1","pages":"dvag022"},"PeriodicalIF":4.3,"publicationDate":"2026-06-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13382199/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148600642","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Characterization of long noncoding RNAs, microRNAs, and piwiRNAs in reef-building corals.","authors":"Jill Ashey, Javier A Rodriguez-Casariego, Kathleen M Durkin, Zachary Bengtsson, Samuel J White, Ariana S Huffmyer, Danielle M Becker, Jose M Eirin-Lopez, Hollie M Putnam, Steven B Roberts","doi":"10.1093/eep/dvag021","DOIUrl":"10.1093/eep/dvag021","url":null,"abstract":"<p><p>Noncoding RNAs (ncRNAs) play critical regulatory roles in gene expression regulation that influence diverse biological processes. Yet, their characterization in nonmodel organisms, particularly sessile, benthic ecosystem engineers such as reef-building corals, remains limited. This study provides the first comprehensive analysis of expressed ncRNAs from three ecologically important coral genera from Mo'orea, French Polynesia: <i>Acropora, Pocillopora</i>, and <i>Porites</i>. We identified homologs for ncRNA biogenesis and functional machinery, characterized long ncRNAs (lncRNAs), microRNAs (miRNAs), and piwiRNAs (piRNAs), and assessed their genomic context and potential targets. Our findings reveal the presence of conserved ncRNA machinery across these coral species, indicating their capability to generate and utilize ncRNAs for gene expression regulation. We identified a single miRNA conserved with corals and Eumetazoans (miR-100), four miRNAs shared across all three species and previously identified in other cnidarian taxa (miR-100, miR-2023, miR-2025, and miR-2036), as well as several species-restricted miRNAs. Predicted gene targets of characterized miRNAs included immune response regulation in <i>A. pulchra</i> and <i>P. tuahiniensis</i> and signal transduction pathways in <i>P. evermanni</i> and <i>P. tuahiniensis</i>. Proximity analysis indicated ~71%-99% of piRNAs overlapped with genes, with genomic maintenance and stability identified as the primary functional enrichment of those genes. lncRNA characterization found little sequence overlap across species (<1%), although lncRNAs in all species were often in proximity to immune-related genes. This study characterizes the genomic features of diverse ncRNAs in reef-building corals and identifies putative regulatory associations between ncRNAs and genes involved in core biological processes.</p>","PeriodicalId":11774,"journal":{"name":"Environmental Epigenetics","volume":"12 1","pages":"dvag021"},"PeriodicalIF":4.3,"publicationDate":"2026-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13343488/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148410973","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"BPA-induced differential methylation of the androgen receptor promoter CpG island in medaka germline and somatic cells.","authors":"Anjana Giri, Jayasree Nath, Ramji K Bhandari","doi":"10.1093/eep/dvag019","DOIUrl":"10.1093/eep/dvag019","url":null,"abstract":"<p><p>The androgen receptors (Ar) are fundamental mediators of androgen signaling, critical for male fertility. Environmental endocrine disruptors (EEDs) can impair male fertility; however, it remains unclear whether EED-induced fertility impairments are linked to DNA methylation alterations in the <i>ar</i> promoter within germ cells, or if a germline-to-soma transfer of these epigenetic profiles affects <i>ar</i> transcription in the testis leading to fertility impairment. To address this, we exposed medaka (<i>Oryzias latipes</i>) to bisphenol A (BPA, 100 µg/l, an EED) and determined fertility defects, testis histology, DNA methylation alterations in the CpG island of <i>arα</i> promoter, and mRNA levels of <i>arα</i> mRNA in the testicular germ cells and soma. Reduced fertility was observed in F0 and F2 generations, which was accompanied by alterations in the testicular tubular structure and germ cell landscape. In F0 males, the testicular germ cells maintained increased levels of DNA methylation on the CpG island of the <i>arα</i> promoter at the ground state of epigenetic reprogramming of germ cells (15 days post-fertilization, dpf) and as such in sperm. In F2 males, testis showed elevated expression of DNA methyltransferase enzyme genes. F2 germ cells maintained significantly higher levels of DNA methylation. The elevated DNA methylation profile was maintained in testicular somatic cells and correlated with significantly decreased <i>arα</i> mRNA levels. The present results demonstrate that ancestral BPA exposure induces transgenerational male subfertility by altering the methylation profile of <i>arα</i> promoter and gene expression, highlighting the profound risk EEDs pose to reproductive health in vertebrates and population stability in wildlife.</p>","PeriodicalId":11774,"journal":{"name":"Environmental Epigenetics","volume":"12 1","pages":"dvag019"},"PeriodicalIF":4.3,"publicationDate":"2026-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13319863/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148367416","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Persistent transcriptomic changes following repeated exposure to wood smoke in nonhuman primate airway epithelial cells.","authors":"Evan Holmes, Anthony P Brown, Sweeney P Elston, Christopher M Royer, Hong Ji","doi":"10.1093/eep/dvag018","DOIUrl":"10.1093/eep/dvag018","url":null,"abstract":"<p><p>Exposure to wildfire smoke is a significant public health concern with the respiratory system heavily impacted. Wildfire events are increasing in number and severity, and inhalation of wildfire smoke can lead to airway inflammation, oxidative stress-induced lung injury, impaired mucociliary clearance, and exacerbation of respiratory conditions such as asthma and chronic obstructive pulmonary disease. Despite these well-documented health risks, the molecular mechanisms underlying the respiratory effects of wildfire smoke exposure and recovery remain incompletely understood. In this study, we utilized transcriptomic and epigenomic analyses to investigate how exposure to wood smoke (WS) influences the expression patterns of gene networks in differentiated tracheobronchial epithelial cells from adult female rhesus monkeys. Our analysis identified exposure-induced differentially methylated regions, differentially expressed genes and gene networks that are implicated in lung disease, including dysregulation of immune responses, oxidative stress, and cell death, compromise of epithelial barrier integrity and function, and epigenetic remodeling. Strikingly, significant transcriptomic changes were still detected one week after exposure cessation, enriched in pathways involved in inflammation, wound healing and tissue repair. Despite these transcriptomic and epigenomic perturbations, histology staining revealed no significant changes in epithelial tissue morphology following WS exposure. However, we found a significant number of pulmonary disease-associated genes and pathways whose transcription were affected by WS exposure. Our study enhances understanding of the molecular basis of wildfire smoke-induced respiratory effects and highlights the potential for WS to leave a lasting imprint on airway epithelium, with important implications for respiratory health in exposed populations.</p>","PeriodicalId":11774,"journal":{"name":"Environmental Epigenetics","volume":"12 1","pages":"dvag018"},"PeriodicalIF":4.3,"publicationDate":"2026-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13317125/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148359975","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"DNA methylation mediates the multiple sclerosis onset risk associated with HHV-6 DNA positivity.","authors":"Alex Eisner, Steve Simpson-Yap, Daniel J Park, Ellen Morwitch, Samuel Tanner, Vicki E Maltby, Ingrid van der Mei, Jeannette Lechner-Scott, Rodney J Scott, Simon A Broadley, Rod A Lea, Pernilla Stridh, Tomas Olsson, Maja Jagodic, Lars Alfredsson, Bruce V Taylor, Anne-Louise Ponsonby","doi":"10.1093/eep/dvag016","DOIUrl":"10.1093/eep/dvag016","url":null,"abstract":"<p><p>In Ausimmune, an Australian multicenter incident case-control study, Epstein-Barr virus (EBV)-related measures, including anti-EBNA antibodies and infectious mononucleosis, show multiple sclerosis (MS) associations mediated by DNA methylation (DNAm). Human herpesvirus-6 (HHV-6) DNA has also been linked to increased MS onset risk, though its mechanisms remain unknown. Therefore, we examined an expanded set of human herpesvirus indices including HHV-6 indices. We first tested associations with MS-associated DNAm modules, then assessed whether HHV-6 DNA contributes to MS onset through DNAm pathways. Serological (serum) and viral load (whole blood) measures of EBV (DNA, viral capsid antigen, early antigen diffuse and restricted), HHV-6 (DNA, IgM, IgG), cytomegalovirus (CMV) (IgG), and varicella zoster virus (DNA, IgG) were collected. DNAm was measured from whole blood (Illumina Infinium Human Methylation EPIC v1). DNAm-module (A1-A5) scores were derived using an epigenome-wide association study for MS onset risk and dimension-reduction methods. A total of 206 cases and 348 matched controls were analyzed. Multivariable linear regression demonstrated associations between HHV-6 DNA positivity and the A2-module, and between higher CMV IgG and the A4 module. Counterfactual mediation analysis indicated that 45% of the positive association of HHV-6 DNA positivity with MS onset risk was mediated through the A2 module (<i>P</i> _indirect = .008). The A2 module showed enrichment for lymphatic and immune pathways. These results provide evidence for a distinct DNAm module as a plausible mechanism underlying the associations of HHV-6 with MS onset. Importantly, these epigenetic pathways appear to mediate associations with human herpesviruses beyond EBV. These findings provide further insights into how environmental factors relate to MS onset through epigenetic programming.</p>","PeriodicalId":11774,"journal":{"name":"Environmental Epigenetics","volume":"12 1","pages":"dvag016"},"PeriodicalIF":4.3,"publicationDate":"2026-05-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13199913/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148028453","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prenatal humid heat exposure and cord blood extracellular vesicle microRNA profiles in a Ghanaian Pregnancy Cohort: GRAPHS.","authors":"Alison Lee, Seyram Kaali, Michelle Li, Mohammed Mujtaba Nuhu, Elena Colicino, Musah Osei, Darby Jack, Sule Awuni, Steven N Chillrud, Haotian Wu, Abigail Gaylord, Cascade Tuholske, Kwaku Poku Asante","doi":"10.1093/eep/dvag017","DOIUrl":"10.1093/eep/dvag017","url":null,"abstract":"<p><p>Humid heat exposures over pregnancy impact birth outcomes but mechanisms are poorly described. We leveraged the Ghana Randomized Air Pollution and Health Study (GRAPHS) to examine associations between maximum shaded wet bulb globe temperature (WBGT) and cord blood extracellular vesicle (EV)-associated microRNA. We also considered heat index (HI) and dry air temperature as secondary exposures. Cord blood was collected at delivery and EVs isolated and RNAs sequenced and small RNA libraries constructed. We assigned participants' trimester and whole pregnancy average heat exposures using satellite reanalysis heat exposures at the level of participant community of residence. We then performed linear regression to examine associations between prenatal heat exposures and log2-transformed miRNA counts and considered significance with an unadjusted <i>P</i>-value ≤ .01 and |beta| > 0.2. In 44 participants, we identified 91 microRNAs that were detected in at least 70% of samples. We identified that miR-146b-5p (β = 0.94 [95% CI = 0.27, 1.6], per 1-degree increase in WBGT); miR-381-3p (β = 2.23 [1.3, 3.15]), miR-378a-3p (β = -1.4, [-2.42, -0.39]), and miR-744-5p (β = 1.51 [0.46, 2.57]); and miR-126-3p (β = -0.75 [-1.2, -0.29]) were associated with first-, second-, and third-trimester WBGT, respectively. miR-1307-3p (β = 2.27 [0.61, 3.94] per 1-degree increase in WBGT) was associated with WBGT averaged over the whole pregnancy. Similar findings were observed with HI. In the GRAPHS cohort, we identified that humid-heat exposure over pregnancy alters the cord blood EV-associated miRNA profiles.</p>","PeriodicalId":11774,"journal":{"name":"Environmental Epigenetics","volume":"12 1","pages":"dvag017"},"PeriodicalIF":4.3,"publicationDate":"2026-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13247845/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148216837","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanistic insights into PM_2.5-induced cardiac fibrosis involving ERS/TXNIP/NLRP3-driven pyroptosis in multiple cell types.","authors":"Siqi Li, Xiaohong Li, Xiaolin Han, Mengxiao Luan, Fengjiao Tan, Yumei Liu, Ruixi Zhou, Wenbo Wu, Chen Liu, Limin Zhang, Qin Wang, Yingjie Zou, Jinfeng Tan, Li Yu, Wanwei Li","doi":"10.1093/eep/dvag015","DOIUrl":"10.1093/eep/dvag015","url":null,"abstract":"<p><p>Fine particulate matter (PM_2.5) exposure leads to cardiovascular diseases (CVDs) by promoting cardiac fibrosis has been demonstrated. However, the mechanisms by which PM_2.5 induces cardiac fibrosis remain unclear. Here, we confirm that the endoplasmic reticulum stress (ERS)/thioredoxin-interacting protein (TXNIP)/nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) signaling pathway is the mechanism of action in PM_2.5-induced cardiac fibrosis, which also plays a crucial role across multiple cell types implicated in this condition. PM_2.5 exposure resulted in increased levels of reactive oxygen species (ROS), the occurrence of ERS, and upregulation of TXNIP expression, as well as pyroptosis and apoptosis in macrophages and cardiomyocytes, subsequently leading to the activation of MCF. The pyroptosis and apoptosis in macrophages and cardiomyocytes, along with MCF activation induced by PM_2.5, were significantly attenuated with the inhibitors of ERS and TXNIP. We also observed that ERS and TXNIP are involved in multiple mechanisms related to oxidative stress and the inflammatory response. We provide insights into the specific mechanisms underlying PM_2.5-induced cardiac fibrosis and suggest potential targets to control PM_2.5-induced cardiac fibrosis.</p>","PeriodicalId":11774,"journal":{"name":"Environmental Epigenetics","volume":"12 1","pages":"dvag015"},"PeriodicalIF":4.3,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13370249/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148455079","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Environmental exposures and epigenetic alterations in common chronic diseases: insights and challenges.","authors":"Cathrine Hoyo, Chantel L Martin, Terrence Allen, David Skaar, Susan K Murphy","doi":"10.1093/eep/dvag014","DOIUrl":"10.1093/eep/dvag014","url":null,"abstract":"<p><p>Exposure to environmental factors including contaminants and social conditions is implicated in a substantial proportion of common non-communicable diseases, and data from model systems repeatedly demonstrate that the process from environmental contributions to common chronic disease risk is mediated through maladaptive epigenetic responses. The field of environmental epigenetics leverages multiple disciplines to advance our understanding of environmental impacts on epigenomic processes to enhance etiologic investigation, guide biomarker discovery, and identify mechanisms of action that ultimately lead to behavioral and or therapeutic interventions. This article discusses examples of emerging research on the links between three common life course exposures linked to common non-communicable diseases, and their associated epigenetic modifications, with a major focus on DNA methylation-the most studied in humans. It also outlines current challenges when interpreting the accumulating body of knowledge, including the lack of consensus on regions reported to be targeted by these environmental exposures. Finally, given that the strongest predictors of epigenetic states are age and cell/tissue type, strategies to build novel platforms using existing technologies to surmount some of these challenges are discussed. Together, these advances in environmental epigenetics are paving the way for groundbreaking developments toward improved precision in developing prevention and intervention strategies to reduce common non-communicable disease morbidity and mortality.</p>","PeriodicalId":11774,"journal":{"name":"Environmental Epigenetics","volume":"12 1","pages":"dvag014"},"PeriodicalIF":4.3,"publicationDate":"2026-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13137992/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147835345","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}