'; ?> geneimprint : Hot off the Press http://www.geneimprint.com/site/hot-off-the-press Daily listing of the most recent articles in epigenetics and imprinting, collected from the PubMed database. en-us Thu, 10 Sep 2026 22:59:09 EDT Thu, 10 Sep 2026 22:59:09 EDT jirtle@radonc.duke.edu james001@jirtle.com Melatonin-enabled omics: understanding plant responses to single and combined abiotic stresses for climate-smart agriculture. Raza A, Li Y, Charagh S, Guo C, Zhao M, Hu Z
GM Crops Food (Dec 2026)

Climate change-driven single and combined abiotic stresses pose escalating threats to sustainable, climate-smart agriculture and global food security. Melatonin (MLT, a powerful plant biostimulant) has established noteworthy potential in improving stress tolerance by regulating diverse physiological, biochemical, and molecular responses. Therefore, this review delivers a comprehensive synopsis of MLT-enabled omics responses across genomics, transcriptomics, proteomics, metabolomics, miRNAomics, epigenomics, phenomics, ionomics, and microbiomics levels that collectively regulate plant adaptation to multiple abiotic stresses. We also highlight the crosstalk between these omics layers and the power of integrated multi-omics (panomics) approaches to harness the complex regulatory networks underlying MLT-enabled stress tolerance. Lastly, we argue for translating these omics insights into actionable strategies through advanced genetic engineering and synthetic biology platforms to develop MLT-enabled, stress-smart crop plants.]]> Wed, 31 Dec 1969 19:00:00 EST The role of RNA modifications in cancer translational control. Joy M, Cleynen A, Shirokikh NE
RNA Biol (Dec 2026)

RNA modifications have emerged as central regulators of cancer translational control. Unlike transcriptional reprogramming, which unfolds over hours, modification-dependent translational rewiring enables rapid proteomic adaptation to the nutrient-deprived, hypoxic, and immunologically hostile tumour microenvironment. Yet most existing reviews organize epitranscriptomic mechanisms by modification type or cancer hallmark, obscuring the mechanistic logic by which chemical marks collectively reshape the translational apparatus. This review adopts a translation-centric framework, examining how the most abundant modifications on mRNAs, tRNAs, and rRNAs regulate each stage of protein synthesis in malignant cells. We survey the epitranscriptomic toolkit, including modification chemistries, enzymatic writers, readers, and erasers, and detection technologies including nanopore direct RNA sequencing. We then trace how modifications control initiation (m6A-driven mRNA circularization, cap-independent translation eIF3 and eIF4G2, rRNA 2'-O-methylation-directed cap-to-IRES switching), elongation (m6A-induced ribosome stalling coupled to mRNA decay, tRNA mcm5s2U-mediated codon-biased translation, YTHDF1-dependent elongation factor recruitment), and termination (pseudouridine-mediated stop codon readthrough, NMD evasion). Crucially, we show that mRNA, tRNA, and rRNA modifications do not act in isolation but form integrated networks. For example, mRNA m6A and tRNA mcm5s2U operate on opposing arms of the same regulatory axis, with direct implications for therapeutic design. We assess the expanding drug pipeline, from the METTL3 inhibitor STC-15 now in Phase 1b/2 trials and METTL3-targeting PROTACs to FTO and ADAR1 inhibitors, and argue that biology-informed combination strategies targeting multiple modification axes will be essential for durable clinical responses.]]> Wed, 31 Dec 1969 19:00:00 EST M6A-dependent regulation of microRNAs from CKD stage 5 patients: insights from epigenetic modification analysis. Yang Z, Liu F, Ye M, Yan Q, Zeng Z, Ma J, Li H, Ma H, Zhang X, Zhu X, Dai Y, Tang D
Epigenetics (Dec 2026)

Chronic kidney disease (CKD) stage 5 is frequently accompanied by systemic inflammation, and peripheral blood mononuclear cells (PBMCs) play an important role. To define the epitranscriptomic features of PBMC small RNAs in CKD stage 5, we profiled N6-methyladenosine (m6A) using small RNA modification microarrays. A total of 158 miRNAs, 149 pre-miRNAs, and 197 tsRNAs showed differential m6A modification. Enrichment analysis implicated PI3K-Akt, p53 signalling, and leukocyte transendothelial migration. Integrating target prediction with GEO transcriptomic datasets identified IRF1 and RUNX2 as key targets. MeRIP confirmed reduced m6A in miR-205-3p and miR-93-5p, accompanied by upregulation of RUNX2 and downregulation of IRF1 by qPCR. These results define an altered m6A-modification profile of PBMC small RNAs in CKD stage 5 and highlight miRNA-target gene axes with potential biomarker utility.]]> Wed, 31 Dec 1969 19:00:00 EST Omics in hereditary optic neuropathies: A systematic review of clinical studies with an integrated point of view. Khanna RK, Cui X, Wong DCS, Makam R, Ducloyer JB, Chao de la Barca JM, Bocca C, Vignal-Clermont C, Blasco H, Orssaud C, Reynier P, Yu-Wai-Man P
Surv Ophthalmol (2026)

Hereditary optic neuropathies are characterized by bilateral visual loss due to the degeneration of retinal ganglion cells, resulting in optic nerve degeneration and atrophy. Although the genetic origin of the main isolated and syndromic hereditary optic neuropathies has been characterized, the clinical phenotypes exhibit significant and poorly understood variability in both penetrance and expressivity. Additionally, the genetic and environmental factors that influence the onset of these optic neuropathies remain poorly understood, with limited biomarkers to predict disease progression or as readouts for therapeutic trials. Data-driven omics strategies allow deep phenotyping to improve our understanding of pathophysiological mechanisms and to search for new biomarkers and therapeutic targets. We explore whether the omics strategies applied to patients with hereditary optic neuropathies have provided such new insights. MEDLINE, Web of Science and EMBASE databases were screened for studies with terms relating to hereditary optic neuropathies, transcriptomics, epigenomics, proteomics, metabolomics and lipidomics in clinical studies exploring patients' samples. Out of 1244 references identified, 22 articles were included after double-masked data curation. These articles focused only on the 3 main forms of hereditary optic neuropathies, namely, OPA1-related dominant optic atrophy (n = 4), Leber hereditary optic neuropathy (n = 13), and Wolfram syndrome (n = 5). While the methodological designs and results of these studies were highly heterogeneous, they revealed molecular alterations that we have attempted to discuss at the integrated multi-omics level. This data integration highlighted several common pathophysiological mechanisms such as energetic impairment, endoplasmic reticulum stress, proteotoxic and oxidative stresses, lipid remodeling and altered amino acid and purine metabolisms, while suggesting potential new biomarkers and therapeutic targets. These findings underscore the potential of integrated multi-omics approaches to deepen our understanding of the phenotypic complexity of hereditary optic neuropathies and to support the development of innovative diagnostic and therapeutic strategies.]]> Wed, 31 Dec 1969 19:00:00 EST Evaluating ancestry adjustment in multi-ancestry epigenome-wide analysis. Liu Y, Kuang A, Hivert MF, Lowe WL, Josefson JL, Scholtens DM
Epigenetics (Dec 2026)

Proper adjustment for population substructure is essential in epigenome-wide association studies (EWAS), particularly in cohorts with diverse ancestries. EPISTRUCTURE offers a genotype-free approach to ancestry inference, originally developed using a European reference population from the Cooperative Health Research in the Region of Augsburg (KORA) study. However, its effectiveness in genetically diverse, multi-ancestry cohorts remains insufficiently evaluated. For EWAS using cord-blood samples from the Hyperglycemia and Adverse Pregnancy Outcome (HAPO) study, we systematically assessed the ancestry adjustment performance of EPISTRUCTURE principal components (PCs) derived from the widely used KORA-based reference set versus new reference sets generated from genotyping data of the multi-ancestry HAPO cohort. HAPO-based reference sets were defined by varying SNP - CpG thresholds (e.g. RS30: ) to identify ancestry-informative CpGs. We applied these reference sets for population substructure adjustment in EWAS of three newborn adiposity traits, birthweight, cord C-peptide, and sum of skinfolds, to evaluate their impact on association detection and biological interpretation. Compared to the KORA reference, the HAPO RS30 reference consistently produced lower genomic inflation and identified more biologically relevant associations for birthweight and cord blood C-peptide in EWAS of HAPO cord blood samples ( = 3,116). Pathway enrichment analyses revealed strong immune and metabolic signals, including pathways uniquely captured by EWAS when using the HAPO-derived reference for ancestry adjustment. Trait enrichment using the EWAS Catalog further confirmed associations with fetal growth, maternal metabolic traits, and glucose regulation. Our findings demonstrate that reference sets derived from multi-ancestry cohorts like HAPO better capture underlying population substructure and improve ancestry adjustment in diverse EWAS settings.]]> Wed, 31 Dec 1969 19:00:00 EST Interactions between nutrition and the epigenome: how can it be harnessed for public health? Anastasopoulou M, Dereki I, Sgourou A, Lagoumintzis G
Future Sci OA (Dec 2026)

A substantial body of evidence shows that dietary habits influence gene expression and epigenetic processes, holding significant implications for public health policies. Epigenetic modifications are increasingly associated with metabolic state, disease risk, and biological aging. Translating mechanistic results into scalable, efficient nutritional epigenetics treatments is difficult.]]> Wed, 31 Dec 1969 19:00:00 EST Global analyses of genomic and epigenomic influences on gene expression reveal as a major regulator of cardiac gene expression in response to catecholamine challenge during heart failure. Lahue C, Ravindran S, Dalal A, Avetisyan R, Rau CD
Epigenetics (Dec 2026)

Heart failure arises from maladaptive remodelling driven by genetic and epigenetic networks. Using a systems genetics framework, we mapped how DNA variants and CpG methylation shape cardiac transcriptomes during beta adrenergic stress in the Hybrid Mouse Diversity Panel, a cohort of over 100 fully inbred mouse strains. Expression QTLs (eQTLs), methylation QTLs (mQTLs) and methylation-driven eQTLs (emQTLs) were generated from over 13k expressed genes and 200k hypervariable CpGs in left ventricles. We discovered hundreds of regulatory 'hotspots' that control large portions of the genome, including several that regulate over 10% of the transcriptome and/or methylome. Approximately 16% of these hotspots overlapped with prior GWAS or EWAS signals. We focus on a hotspot on chromosome 12 and identify the serpine peptidase inhibitor , as the most likely driver gene in this hotspot. Experimental knockdown of in neonatal rat ventricular cardiomyocytes blunted hypertrophy induced by a variety of hypertrophic signals, while altering predicted target expression and modulating the activity of and . Together, these findings position as a major regulator of stress-responsive cardiac gene programs, highlighting how integration of genetic and epigenetic signals can pinpoint key drivers of heart failure.]]> Wed, 31 Dec 1969 19:00:00 EST Computational advances in epigenetic regulation databases and prediction tools. Yang L, Yang M, Li X, Zhou X, Wang Z, Zhou K, Xie L, Chen F, Chen G, Liu S
Biotechnol Adv (Nov 2026)

Epigenetic regulation refers to heritable changes in gene expression without altering the DNA sequence. It mainly includes DNA methylation, histone modification, RNA modification and non-coding RNAs (ncRNAs). Abnormalities in epigenetic regulation play a key role in the development of many diseases. In recent years, with the rapid development of high-throughput sequencing technology, epigenetic modification datasets have accumulated rapidly, which has facilitated the development of various database resources and computational analysis tools. At the same time, the emergence of artificial intelligence technologies such as machine learning and deep learning has further improved the speed and accuracy of epigenetic modification site prediction and functional mining. However, most existing reviews focus on databases and computational tools for single types of epigenetic modifications, whereas systematic overviews of integrated databases, multi-algorithm prediction tools, and applications of artificial intelligence technologies in this field remain scarce. Here, we systematically introduce the current major databases and prediction tools for DNA methylation, histone modification, RNA modification, ncRNAs, and disease-related epigenetic modifications, highlighting the potential of artificial intelligence technologies, including deep learning, in epigenetic modification research and pharmaceutical research. In addition, we discuss the challenges faced by existing computational methods in the field and future directions, providing references for data repositories and computational tools selected by researchers, as well as new insights into epigenetic mechanism studies.]]> Wed, 31 Dec 1969 19:00:00 EST Nanopore-based epigenomic profiling reveals the absence of widespread CpG methylation in the African swine fever virus genome. Wu X, Guo Z, Shao Y, Wang X, Li R
Microbiol Res (Dec 2026)

DNA methylation is a critical epigenetic mechanism implicated in regulating replication and transcription in DNA viruses. However, the epigenetic landscape of African swine fever virus (ASFV), a large double-stranded DNA virus infecting pigs, remains controversial. Here, we systematically profiled the DNA methylome of the first ASFV strain isolated in Hong Kong (HK_NT_202103) using Oxford Nanopore Technologies (ONT) R10.4.1 sequencing. We employed a paired design: native whole-genome sequencing (WGS) against a methylation-free whole-genome amplification (WGA) control. Using conservative thresholds, we found no evidence of 5-methylcytosine (5mC), especially typical CpG methylation, across the viral genome. Importantly, clear CpG methylation signals were successfully detected in the host genome from WGS data, confirming the functionality of the workflow to detect 5mC at CG sites. While widespread 5mC seems absent, a small number of putative N-methyladenine (6mA) loci were identified. A specific 6mA candidate exhibited raw ionic current disruptions and gene-level intersection with another ASFV isolate (CAS19-01/2019), although it lacked single-base consensus across different methylation callers or between the two isolates. Although our biological findings are restricted to a single isolate under specific experimental conditions, this study introduces a novel, highly rigorous ONT framework for viral epigenomics research. Furthermore, the absence of ASFV CpG methylation indicates that host CpG-depletion remains a viable strategy for viral metagenomic enrichment. Ultimately, our work offers a critical methodological baseline for ASFV surveillance and highlights the necessity of targeted experimental validation for rare viral modifications.]]> Wed, 31 Dec 1969 19:00:00 EST Multi-omic biomarkers in cardiovascular disease: Discovery to clinical translation. AlRamadneh TN, Abdulsahib WK, Gajjar TB, Hanumanthayya M, Shukla SK, Panigrahi R, Bainsal N, Rizaev J, Abduvoyitov B, Polatova D
Clin Chim Acta (Jan 2027)

Cardiovascular disease (CVD) remains the leading cause of mortality worldwide, necessitating improved risk stratification and early detection strategies. Multiomics approaches that integrate genomics, transcriptomics, proteomics, metabolomics, and epigenomics offer unprecedented opportunities for biomarker discovery and precision medicine in cardiovascular care. This narrative review examines the current landscape of multiomics biomarkers for CVD, tracing their evolution from discovery to clinical translation. We synthesize evidence from recent studies evaluating the clinical utility of integrated omics approaches across diverse cardiovascular conditions, including atherosclerotic cardiovascular disease, heart failure, and atrial fibrillation. High-throughput proteomics has identified novel protein signatures that enhance cardiovascular risk prediction beyond traditional risk factors. Metabolomics has revealed pathway-specific biomarkers, including trimethylamine N-oxide and lipid species, associated with atherogenesis. Polygenic risk scores derived from genomic data demonstrate incremental value when combined with clinical risk scores. Multiomics biomarkers represent a transformative approach to cardiovascular risk assessment and disease management.]]> Wed, 31 Dec 1969 19:00:00 EST Translational reprogramming of TGF-β signaling via TRMT61A-mediated tRNA mA drives prostatic fibrosis and hyperplasia. Liu Y, Yu L, Zhang H, Huang R, Liao X, Liu Y, Mei H
Cell Signal (Dec 2026)

Dysregulation of the epitranscriptomic landscape is closely linked to pathological proliferation, but its specific role in benign prostatic hyperplasia (BPH) remains unclear. Here, we identify the tRNA methyltransferase TRMT61A as a critical driver of BPH progression. We found that TRMT61A and global N1-methyladenosine (mA) levels are aberrantly upregulated in human BPH tissues. Functionally, TRMT61A knockdown potently suppresses prostate cell proliferation and reduces stromal fibrosis, inducing G1 cell cycle arrest and reversing pathological remodeling both in vitro and in vivo. By integrating ribosome profiling (Ribo-seq) and tRNA-seq, we observed that TRMT61A drives translational reprogramming. TRMT61A preserves the stability of specific tRNA isoacceptors (e.g., tRNA-Leu-CAA), which is required for the efficient decoding of mRNAs containing mA-dependent codons. Consequently, TRMT61A selectively promotes the translational elongation of the key receptor TGFβR1. This amplifies downstream TGF-β/SMAD signaling and drives epithelial-mesenchymal transition (EMT) without affecting mRNA transcription. In summary, our study reveals how TRMT61A drives BPH progression through TGFβR1 translation, highlighting the therapeutic potential of targeting epitranscriptomic pathways to reverse prostatic hyperplasia and fibrosis.]]> Wed, 31 Dec 1969 19:00:00 EST Epitranscriptomic erasers in bivalves: Evolutionary divergence and species-specific transcriptional plasticity of the ALKBH family under acute thermal stress. Xiong D, Li Y, Hu H, He Q, Su H, Liao W, Xu T, Xu C, Zhang H, Zheng H
Comp Biochem Physiol Part D Genomics Proteomics (Dec 2026)

The AlkB homolog (ALKBH) family of Fe(II)/α-ketoglutarate-dependent dioxygenases mediates nucleic acid demethylation, thereby governing RNA metabolism and genomic stability. Despite their pivotal roles in epitranscriptomic regulation across vertebrates, the evolutionary dynamics and functional significance of ALKBH proteins in bivalve mollusks remain largely unexplored. Here, we present a comprehensive phylogenomic analysis of 210 ALKBH genes identified across 35 bivalve species. Our analyses reveal a distinct evolutionary trajectory characterized by the lineage-specific loss of ALKBH4 and the restricted distribution of ALKBH5 to the Mytilidae family, contrasting sharply with vertebrate repertoires. Using the noble scallop (Chlamys nobilis) and Pacific oyster (Crassostrea gigas) as model systems, we demonstrate that ALKBH genes exhibit conserved spatiotemporal expression patterns, with pronounced enrichment in gonadal tissues and during metamorphic transitions, implicating these enzymes in gametogenesis and larval development. Furthermore, comparative thermal stress experiments reveal divergent transcriptional plasticity: the subtropical scallop C. nobilis mounts rapid, transient induction of ALKBH1/2/6 under heat shock, whereas the eurythermal oyster C. gigas maintains sustained ALKBH3 expression, potentially underpinning its superior thermal tolerance. Conversely, cold stress elicits bimodal regulation in C. nobilis, with ALKBH1/2 upregulation contrasting with ALKBH6/7/8 suppression. These findings illuminate the functional diversification of bivalve ALKBH genes and their potential utility as molecular biomarkers for assessing developmental competence and thermal resilience in shellfish aquaculture.]]> Wed, 31 Dec 1969 19:00:00 EST Integrative multi-omics reveals a fibroblast-centered, ZFHX3-prioritized regulatory framework linking sick sinus syndrome and atrial fibrillation. Yan Z, Pu X, Cai Y, Wu Q, Chang X, Zhang X, Wang Y, Liu J, Liu Z, Liu R
Cell Signal (Dec 2026)

To define shared genetic and multi-scale mechanisms underlying comorbidity between sick sinus syndrome (SSS) and atrial fibrillation (AF).]]> Wed, 31 Dec 1969 19:00:00 EST Advanced deep learning strategies in nanopore RNA sequencing. Ling C, Lebeau B, Keong KC, Fullwood M
RNA Biol (Dec 2026)

The epitranscriptome comprises chemical modifications found on RNA molecules that play essential roles in co- and post-transcriptional gene regulation. Dysregulation of these modifications has been implicated in various diseases, fuelling interest in evaluating them as emerging biomarkers and therapeutic targets. Nanopore direct RNA sequencing provides a powerful platform for profiling diverse RNA modifications at single-molecule resolution, but the complexity of the signals requires advanced computational approaches for interpretation. Artificial intelligence, particularly deep learning (DL), has become central to this effort. While classical DL architectures such as convolutional and recurrent neural networks have been widely applied, more recent approaches employ specialized learning frameworks and ensemble strategies to address challenges of data scarcity, noise, and biological variability while providing higher resolution output. In this review, we summarize these developments and highlight future multidisciplinary opportunities at the intersection of artificial intelligence and biology for characterizing the epitranscriptome obtained with direct RNA nanopore sequencing.]]> Wed, 31 Dec 1969 19:00:00 EST Culture-dependent decoupling of allele-specific expression from :IG-DMR methylation in experimental models. Selenou C, Brioude F, Sudre L, Pham A, Netchine I, Sobrier ML, Giabicani Ã‰
Epigenetics (Dec 2026)

Genomic imprinting is an epigenetic mechanism leading to the monoallelic expression of a subset of genes, mainly regulated by DNA methylation at imprinting control regions (ICRs). Silver-Russell syndrome (SRS) is a paradigmatic imprinting disorder in which loss of methylation at the 11p15.5 :IG-DMR is associated with downregulation of and biallelic expression of . Currently, the allele-specific expression of imprinted genes is widely inferred from ICR methylation without direct assessment. Here, we quantified allele-specific expression together with :IG-DMR methylation in control ( = 32) and SRS ( = 12) samples spanning tissues and commonly used cellular models, including fibroblasts, induced pluripotent stem cells (iPSCs) and dental pulp stem cells (DPSCs). Overall, allele-specific expression was concordant with :IG-DMR methylation in tissues, iPSCs and fibroblasts, with clear allelic bias in controls and predominantly biallelic expression in SRS samples. Nevertheless, some SRS-derived fibroblast lines retained an allelic bias despite loss of methylation. In addition, a subset of control DPSCs with balanced methylation exhibited biallelic expression. We showed that the observed decoupling between methylation and allele-specific expression was associated with culture-related procedures, including repeated passaging and freeze-thaw cycles in DPSCs. These findings show that ICR methylation does not always faithfully reflect imprinted gene expression and therefore cannot be uncritically used as a proxy for imprinting. They further indicate that culture-related procedures can promote loss of imprinting and support the systematic combined assessment of ICR DNA methylation and allele-specific expression when establishing cellular models for imprinting disorders.]]> Wed, 31 Dec 1969 19:00:00 EST A cell type enrichment analysis tool for brain DNA methylation data (CEAM). Müller J, Laroche VT, Imm J, Weymouth L, Harvey J, Reijnders RA, Smith AR, van den Hove D, Lunnon K, Cavill R, Pishva E
Epigenetics (Dec 2026)

DNA methylation (DNAm) signatures are highly cell type-specific, yet most epigenome-wide association studies (EWAS) are performed on bulk tissue, potentially obscuring critical cell type-specific patterns. Existing computational tools for detecting cell type-specific DNAm changes are often limited by the accuracy of cell type deconvolution algorithms. Here, we introduce CEAM (Cell-type Enrichment Analysis for Methylation), a robust and interpretable framework for cell type enrichment analysis in DNA methylation data. CEAM applies over-representation analysis with cell type-specific CpG panels from Illumina EPIC arrays derived from nuclei-sorted cortical post-mortem brains from neurologically healthy aged individuals. The constructed CpG panels were systematically evaluated using both simulated datasets and published EWAS results from Alzheimer's disease, Lewy body disease, and multiple sclerosis. CEAM demonstrated resilience to shifts in cell type composition, a common confounder in EWAS, and remained robust across a wide range of differentially methylated positions, when upstream modeling of cell type composition was modeled with sufficient accuracy. Application to existing EWAS findings generated in neurodegenerative diseases revealed enrichment patterns concordant with established disease biology, confirming CEAM's biological relevance. The workflow is publicly available as an interactive Shiny app (https://um-dementia-systems-biology.shinyapps.io/CEAM/) enabling rapid, interpretable analysis of cell type-specific DNAm changes from bulk EWAS.]]> Wed, 31 Dec 1969 19:00:00 EST N6-methyladenosine modification of mRNAs in retinal ischemia-reperfusion in mice. Liang J, Li Y, Wen Y, Li Z, Deng C, Zhuo Y, Li Y, Zhu Y
Epigenetics (Dec 2026)

Retinal ischemia-reperfusion injury (RIR) is the main pathogenic mechanisms of acute glaucoma, diabetic retinopathy, central retinal vein occlusion. As a common post-transcriptional modification of eukaryotic RNAs, N6-methyladenosine (mA) is associated with the pathogenesis of different diseases, including angiogenesis, through the regulation of RNA metabolism and functions. The aim of this study was to identify the potential relevance of mA RNA methylation in pathogenesis of RIR. A total of 10,851 mRNAs and 23,270 associated mA methylation modified peaks were identified in the RIR group. Similarly, 10,391 mRNAs and 22,935 associated mA methylation modified peaks were detected in the Sham group. MeRIP-seq identified 3,871 RIR-specific mA peaks and 3,624 Sham-specific mA peaks, in addition to 19,399 shared peaks between groups. Gene ontology (GO) analysis showed that hypermethylated mRNAs were enriched in cellular process, cellular anatomical entity, and binding, while hypomethylated mRNAs were enriched in synaptic signaling, synapse, and gated channel activity. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis indicated that hypermethylated mRNAs were involved in tight junction, hippo signaling pathway, and PI3K-Akt signaling pathway, while hypomethylated mRNAs were involved in Neuroactive ligand-receptor interaction, glutamatergic synapses, cholinergic synapses. Joint analysis identified mRNAs with differential mA methylation and expression simultaneously. Among them, the expression patterns of , , and were confirmed by RT-qPCR to be consistent with the sequencing results. The results revealed an altered mA epitranscriptome in RIR retinas. These methylated RNAs may act as novel modulators and targets in RIR.]]> Wed, 31 Dec 1969 19:00:00 EST Multi-omics panorama of glaucoma: Pathogenesis, biomarkers, and novel therapeutic strategies. Gao J, Liu M, Liu X, Zhang M, Qu W, Wang W, Cao P, Mo Y
Surv Ophthalmol (2026)

Glaucoma is a group of irreversible, blinding eye diseases characterized by progressive loss of retinal ganglion cells, leading to gradual visual field defects that severely impact patients' quality of life. Its complex pathophysiological mechanisms remain incompletely understood, limiting the development of early diagnostic and effective therapeutic strategies. Advances in omics technologies have provided new insights into elucidating the pathophysiology of glaucoma. We summarize specific alterations in genomics, transcriptomics, proteomics, metabolomics, epigenomics, and microbiomics associated with glaucoma. We emphasize the systematic analysis of disease mechanisms, identification of clinically applicable biomarkers, and discovery of novel therapeutic targets through the integration of these data. This approach paves new pathways for glaucoma subtype diagnosis and personalized treatment, while also outlining future research directions and challenges.]]> Wed, 31 Dec 1969 19:00:00 EST Epigenetic regulation of vertebrate limb development: from field specification to tissue morphogenesis. Vallejo-De Lira CM, Galván-Hernández CI, Chimal-Monroy J, Marin-Llera JC
Epigenetics (Dec 2026)

Vertebrate limb development provides an excellent model for understanding how epigenetic mechanisms coordinate the integration of positional information and temporal signals to generate complex three-dimensional structures. An increasing body of evidence shows that chromatin-based mechanisms, including DNA methylation, histone modifications, and higher-order chromatin organization, define the competence of progenitor cells to respond to morphogenetic signals with spatial and temporal precision during limb development. This review explores how epigenetic mechanisms orchestrate and regulate the major phases of limb formation: from field specification and bud induction to morphogenesis, lineage differentiation, and programmed cell death. Here, we examine how chromatin remodeling, histone and DNA modifications, and enhancer - promoter interactions functionally converge with developmental signaling pathways to control gene expression programs that govern timing, positional identity, and cell fate decisions. Furthermore, this review highlights recent advances that link epigenetic landscapes with morphogenetic outcomes and discusses how comparative epigenomic approaches are reshaping our understanding of evolutionary diversification in limb morphology.]]> Wed, 31 Dec 1969 19:00:00 EST Analysis of the dual role of amyloid-beta in Alzheimer's disease through multi-omics integration. Guo J, Lu X, Qiu L, Xue W, Fu H, Wang K, Wang Y
Neural Regen Res (Nov 2026)

Accumulation of amyloid-beta is highly important in the development of Alzheimer's disease. Given the limitations of the amyloid cascade hypothesis and the repeated clinical failures of anti-amyloid-beta therapies, researchers are increasingly exploring the infection hypothesis. This review explores the dual behaviors of amyloid-beta in Alzheimer's disease, with a particular focus on its protective role against infection by microorganisms and its complicated connections with innate immune system. This new opinion holds that amyloid-beta can play an antimicrobial peptide role. During microbial invasion, its original role is to protect neural tissue, but prolonged accumulation leads to chronic deposition and involvement in pathological processes. Evidence from in vitro experiments, animal models, and clinical studies indicates that amyloid-beta may possess antiviral and antibacterial properties, particularly against infections such as herpes simplex virus, human immunodeficiency virus, and Porphyromonas gingivalis . However, excessive accumulation of amyloid beta triggers a neuroinflammatory cascade that impairs neuronal regeneration and cognitive function. Despite substantial research into Alzheimer's disease, current treatments have not yielded significant clinical benefits. Although monoclonal antibodies such as Aducanumab , Lecanemab , and Donanemab have been approved for marketing, their strict indications and high costs pose challenges for widespread promotion. The infection hypothesis of amyloid-beta has spurred clinical trials investigating vaccines targeting specific pathogens to assess their potential in preventing or treating Alzheimer's disease. This highlights the need for further exploring the multifaceted role of amyloid-beta in Alzheimer's disease. In addition, microbial infections can also trigger or regulate genetic and epigenetic factors, accelerating amyloid beta deposition. Among them, the apolipoprotein E epsilon 4 allele is the strongest genetic risk factor for Alzheimer's disease, as it exacerbates the accumulation of amyloid beta and promotes neuroinflammation. Strategies targeting epigenetic regulation may provide novel approaches to inhibit Alzheimer's disease pathology. This review also integrates various technologies such as genomics, proteomics, and metabolomics. This provides a broader system-level understanding of the risk gene loci, protein interaction networks, and metabolic changes associated with amyloid beta under the influence of microbial infections. Such techniques may lead to the identification of new molecular targets, the development of individualized treatment strategies, and the creation of early biomarkers for use in clinical research. In conclusion, this review suggests that amyloid-beta is not merely a pathological by-product but an environmentally responsive molecule with dual functions. A deeper understanding of the dynamic regulation of amyloid-beta, considering infection status and disease stage, can provide new directions for treatment strategies aimed at the prevention and treatment of Alzheimer's disease.]]> Wed, 31 Dec 1969 19:00:00 EST