Diabetic cardiomyopathy (DbCM), a complex metabolic disease, greatly threatens human health due to therapeutic limitations. Multi-omics approaches facilitate the elucidation of its intrinsic pathological changes.

Histone deacetylase 3 (HDAC3) is a critical regulator of gene expression, influencing a variety of cellular processes in the central nervous system. As such, dysfunction of this enzyme may serve as a key driver in the pathophysiology of various neuropsychiatric disorders and neurodegenerative diseases. HDAC3 plays a crucial role in regulating neuroinflammation, and is now widely recognized as a major contributor to neurological conditions, as well as in promoting neuroprotective recovery following brain injury, hemorrhage and stroke. Emerging evidence suggests that pharmacological inhibition of HDAC3 can mitigate behavioral and neuroimmune deficits in various brain diseases and disorders, offering a promising therapeutic strategy. Understanding HDAC3 in the healthy brain lays the necessary foundation to define and resolve its dysfunction in a disease state. This review explores the mechanisms of HDAC3 in various cell types and its involvement in disease pathology, emphasizing the potential of HDAC3 inhibition to address neuroimmune, gene expression and behavioral deficits in a range of neurodegenerative and neuropsychiatric conditions.

To investigate DNA methylation levels of a panel of genes in thymic epithelial tumors (TETs). We selected 15 genes among the most promising epigenetic biomarkers of TETs and evaluated their methylation levels in 71 TET samples. thymic carcinomas (TCs) showed hypermethylation of and genes and reduced methylation levels compared with thymomas (TMs) and healthy thymic tissues. was hypomethylated in TMs compared with healthy thymic tissues. No difference in the methylation levels of the investigated genes was seen among TM stages and subtypes. No changes in blood methylation levels of the investigated genes were seen among TET subtypes. The present study confirms and as TET epigenetic biomarkers.

Our understanding of the origins of noncommunicable diseases has evolved over the years with greater consideration given to the lasting influence exposures and experiences during the preconceptional and prenatal periods can have. Research highlights the associations of parental exposures (e.g., diet, obesity, gestational diabetes, lipid profile, toxic exposures and microbiome) with the infant/fetal methylome and suggest associations with infant, child and/or adolescent chronic health outcomes. Thus, epigenetics and specifically cord blood DNA methylation may have utility as biomarkers for disease risk identification and stratification in pediatrics. However, for cord blood DNA methylation analyses to be leveraged as biomarkers of disease risk in pediatric clinical practice, the results must be replicable, validated and clinically meaningful. Challenges and opportunities to this prospect are herein discussed.

Exposure to pollutants and chemicals during critical developmental periods in early life can impact health and disease risk across the life course. Research in environmental epigenetics has provided increasing evidence that prenatal exposures affect epigenetic markers, particularly DNA methylation. In this article, we discuss the role of DNA methylation in early life programming and review evidence linking the intrauterine environment to epigenetic modifications, with a focus on exposure to tobacco smoke, metals, and endocrine-disrupting chemicals. We also discuss challenges and novel approaches in environmental epigenetic research and explore the potential of epigenetic biomarkers in studies of pediatric populations as indicators of exposure and disease risk. Overall, we aim to highlight how advancements in environmental epigenetics may transform our understanding of early-life exposures and inform new approaches for supporting long-term health.

Epigenetic dysregulation is an important nexus in the development and maintenance of human cancers. This review provides an overview of how understanding epigenetic dysregulation in cancers has led to insights for novel cancer therapy development. Over the past two decades, significant strides have been made in drug discovery efforts targeting cancer epigenetic mechanisms, leading to successes in clinical development and approval of cancer epigenetic therapeutics. This article will discuss the current therapeutic rationale guiding the discovery and development of epigenetic therapeutics, key learnings from clinical experiences and new opportunities on the horizon.

To describe tDRs in human milk EVs and their associations with maternal body mass index, age, dietary indices, breastfeeding frequency, season and time of milk collection in a Latina population.

Over the past century, human lifespan has increased remarkably, yet the inevitability of aging persists. The disparity between biological age, which reflects pathological deterioration and disease, and chronological age, indicative of normal aging, has driven prior research focused on identifying mechanisms that could inform interventions to reverse excessive age-related deterioration and reduce morbidity and mortality. DNA methylation has emerged as an important predictor of age, leading to the development of epigenetic clocks that quantify the extent of pathological deterioration beyond what is typically expected for a given age. Machine learning technologies offer promising avenues to enhance our understanding of the biological mechanisms governing aging by further elucidating the gap between biological and chronological ages. This perspective article examines current algorithmic approaches to epigenetic clocks, explores the use of machine learning for age estimation from DNA methylation, and discusses how refining the interpretation of ML methods and tailoring their inferences for specific patient populations and cell types can amplify the utility of these technologies in age prediction. By harnessing insights from machine learning, we are well-positioned to effectively adapt, customize and personalize interventions aimed at aging.

Mammalian genomes encode 12 proteins that contain a CXXC zinc finger domain. Most members of this family are large multi-domain proteins that function in the control of DNA methylation and histone methylation patterns. CXXC5 is a smaller member of the family, along with its closest homologue CXXC4. These two proteins lack known catalytic domains. Here, we have characterized CXXC5 in mouse embryonic stem (ES) cells.

Aging presents a significant challenge to health and social care systems due to the increasing proportion of the elderly population. The identification of reliable biomarkers to assess the progression of aging remains an unresolved question. Circular RNAs (circRNAs) are single-stranded covalently closed RNAs. They have been found to regulate various biological processes. CircRNAs are present in human biological fluids, are relatively stable, and accumulate with age, making them promising as biomarkers of aging. Current information on the expression of circRNAs in aging was analyzed using scientific databases. In this review, we have identified key stages in the study of circRNAs during aging and summarized the current understanding of their biogenesis. By focusing on the role of circRNAs in processes that contribute to aging - such as genomic stability, metabolism, cell death, and signaling pathways - we hypothesize that circRNAs may drive the aging process through their age-related accumulation and resultant deregulation. Examples of age-related differential expression of circRNAs in various species, including humans, are provided. This review highlights the importance of finding novel epigenetic biomarkers of aging, beyond the already identified molecules (circFOXO3, circRNA100783, circPVT1), and highlights circRNAs as a potential therapeutic target for the treatment of age-associated diseases.

Existing analyses with conventional assays have generated significant insights into static states of DNA methylation but were unable to visualize the dynamics of epigenetic regulation.

Neurofibromatosis (NF) is identified as genetic disorder characterized by multiple tumors on nerve tissues. NF1 is the most prevalent form, identified by neurofibromas and skin changes. NF1 is the most prevalent neurofibromatosis disorder, distinct from the rarer NF2 and schwannomatosis (SWN) conditions. NF2, including NF2-related SWN (NF2-SWN), predominantly involves schwannoma formation and differs from in its genetic basis and clinical presentation. Despite the established genetic basis of NF, effective treatments remain scarce. Long non-coding RNAs (lncRNAs) have emerged as important regulators of gene expression, impacting pathways vital to tumor biology. This review explores the lncRNAs role in NF pathogenesis along with their potential as therapeutic targets. LncRNAs such as and show dysregulated expression in NF, influencing signaling pathways like Ras/MAPK and JAK/STAT, thereby contributing to tumor development. Understanding these interactions sheds light on the molecular mechanisms underlying NF and highlights lncRNAs as potential biomarkers of diagnosis and prognosis of NF. Additionally, therapeutic strategies targeting lncRNAs with antisense oligonucleotides (ASOs) or CRISPR-Cas9 offer promising treatment options. The present review emphasizes crucial role of lncRNAs in NF pathogenesis and their promise to create innovative treatments, aiming to improve patient outcomes and meet the urgent need for effective NF therapies.

DNA methylation is associated with gastric cancer and () infection, while increasing evidence indicated involvement of other microbes reside in gastric mucosa during gastric tumorigenesis. We investigated bacterial communities in the gastric mucosa accompanied with related methylation anomaly. Gastric mucosa samples from antrum were obtained from 182 cancer-free patients. Bacterial communities were evaluated using 16S rRNA sequencing. The result was correlated with related promoter CpG island (CGI) methylation of five genes (), LINE1 hypomethylation and telomere length. We showed correlation between lower bacterial alpha diversity and higher CGI methylation. Multivariate analysis demonstrated older age (t = 3.46,  = 0.0007), infection (t = 9.99,  < 0.0001) and lower bacterial alfa diversity (Shannon index: t = -2.34,  = 0.02) were significantly associated with CGI hypermethylation. In genus or family levels, increased abundance of was associated with hyper CGI methylation with strongest correlation, while decreased abundance of four bacteria (, and ) was also associated with hyper CGI methylation. Our findings suggest the potential correlation between CGI methylation induction and lower bacterial alpha diversity in the gastric mucosa accompanied by infection.

To investigate mechanism of lncRNA SNHG12 induced macrophage-myofibroblast transition (MMT) in cancer-associated fibroblasts (CAFs)-derived extracellular vesicles (EVs) in non-small cell lung cancer (NSCLC).

nc886 is a regulatory noncoding RNA that is transcribed by RNA polymerase III (Pol III), is variably expressed in different biological contexts, and plays roles in inflammation and cancer. Epigenetic mechanisms play an intriguing role in regulating nc886 expression. As a maternally imprinted gene and metastable epiallele, nc866 exhibits polymorphic imprinting, with a methylation status that is influenced by environmental and biological factors. Consequently, the promoter DNA methylation status and the different resulting RNA expression levels of nc886 are associated with physiological and pathological conditions. In this review, we summarize the literature and explore the significance in relation to diverse roles of nc886.

A complex interaction among sensory, social and epigenetic determinants in psychiatric conditions was described across all age strata. The high prevalence of mental disorders in individuals with sensory deficits might be attributed to the interaction among social isolation, cognitive functioning and sensory processing. The epigenetic implications of such interactions were examined: environmental and social factors can affect gene expression and impact the pathogenesis of psychiatric disorders also through sensory processing. This article discussed the role of social determinants, in other words, social isolation, loneliness and chronic stress, in promoting psychiatric disorders and, in a vicious circle, sensory deficits (vision, hearing, olfaction and somatosensation). We emphasized the importance of integrating social, sensory and epigenetic factors to target different treatments for psychiatric conditions.

To explore precise function and underlying mechanism of circ_0006988 in gastric cancer (GC). GC tissues were collected clinically, and GC cells were purchased from the company. Quantitative real-time polymerase chain reaction and western blot were used to detect mRNA and protein expression. Functional analysis was performed through CCK-8, Transwell and scratch experiment. Binding relationship was validated through dual luciferase reporter and RNA immunoprecipitation assays. HGC-27 cells were subcutaneously injected into mice to construct a xenograft tumor model. In GC tissues and cells, circ_0006988 overexpressed, promoting proliferation, migration and invasion. MiRNA-92a-2-5p downregulation or overexpression weakened effects of circ_0006988 silencing on GC progression. circ_0006988 facilitates GC development through miRNA-92a-2-5p/TFAP4 axis.

Inborn errors of immunity (IEIs) are a group of typically monogenic disorders characterized by dysfunction in the immune system. Individuals with these disorders experience increased susceptibility to infections, autoimmunity and malignancies due to abnormal immune responses. Epigenetic modifications, including DNA methylation, histone modifications and chromatin remodeling, have been well explored in the regulation of immune cell development and effector function. Aberrant epigenetic modifications can disrupt gene expression profiles crucial for immune responses, resulting in impaired immune cell differentiation and function. Dysregulation of these processes caused by mutations in genes involving in epigenetic modifications has been associated with various IEIs. In this review article, we focus on IEIs that are caused by mutations in 13 genes involved in the regulation of DNA methylation, histone modification and chromatin remodeling.