'; ?> 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 Wed, 17 Jun 2026 15:18:39 EDT Wed, 17 Jun 2026 15:18:39 EDT jirtle@radonc.duke.edu james001@jirtle.com Epigenomic profiling of neuroendocrine lung cancers identifies a classical-neuroendocrine ASCL1/NKX2-1 subtype and a SOX11-associated differentiation axis linked to reduced immunogenicity. Sato T, Hamamoto J, Emoto K, Nagashio R, Yagami Y, Yamamoto H, Inoue R, Matsuo H, Shirasawa M, Kuchitsu Y, Kawano S, Hara Y, Yoo S, Fukushima T, Sugihara K, Terai H, Sanoyama I, Murakumo Y, Domoto H, Haraguchi-Hashiguchi M, Shiomi K, Mikubo M, Yasuda H, Watanabe H, Naoki K
Lung Cancer (Jul 2026)

Heterogeneity of neuroendocrine (NE) differentiation in pulmonary high-grade NE carcinoma, mainly small-cell lung cancer (SCLC), has been recently explored based on the expression of lineage transcription factors such as ASCL1, NEUROD1 and POU2F3. However, molecular classification based on these factors remains incomplete, and NE differentiation in lung cancers is more heterogeneous than previously appreciated. Here, we investigated the heterogeneity of NE differentiation using epigenomic profiling across a range of lung cancers with NE components, predominantly large-cell neuroendocrine carcinoma (LCNEC).]]> Wed, 31 Dec 1969 19:00:00 EST Bridging the gaps in Alzheimer's disease biomarker research: From multi-omics integration to point-of-care diagnostics, a comprehensive review. Khasanov S, Tolibov M, Daminova N
Clin Chim Acta (Jul 2026)

Alzheimer's disease (AD) is the most prevalent neurodegenerative disorder, yet its early and definitive diagnosis remains a formidable clinical challenge. Over the past decade, substantial progress has been made in the identification and validation of AD biomarkers across cerebrospinal fluid (CSF), blood, and emerging non-invasive biofluids. The core CSF biomarkers-amyloid-β (Aβ42), total tau (t-tau), and phosphorylated tau (p-tau)-have been integrated into revised diagnostic criteria, while blood-based biomarkers such as plasma p-tau217 and the Aβ42/Aβ40 ratio are approaching clinical readiness. Simultaneously, electrochemical biosensor technologies have demonstrated remarkable detection sensitivity at the femtomolar level, and multi-omics approaches combining metabolomics, lipidomics, proteomics, and epigenomics are revealing new molecular signatures of early AD. Despite these advances, several critical research questions remain unanswered, including how to optimally combine biomarkers across biofluids, how to translate biosensor technology from the laboratory to the clinic, how to integrate multi-omics data into practical diagnostic frameworks, how to validate non-invasive biofluid markers at clinical scale, and how to harmonize blood-based assays for global implementation. This review systematically examines the current state of AD biomarker science, identifies key unresolved challenges, evaluates the most promising existing approaches, and proposes specific methodological strategies to advance the field from discovery to clinical practice.]]> 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 Beyond Weight: Systems Biology and Precision Medicine Redefine Obesity as a Multidimensional Disease. Liu Y, Yang Y, Zhu L, Peng W
Diabetes Obes Metab (Jul 2026)

Traditional weight-centered models do not fully capture the biological complexity of obesity. Systems biology offers a new framework by integrating molecular, cellular, clinical, and environmental information to reframe obesity as a heterogeneous, multidimensional disease.]]> 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 Epigenetic research methods and animal models for intervertebral disc degeneration (Review). Cui X, Zeng L, Zhang W, Xi L, Wang R, Jia D, Safa , Feng H, Jia H
Mol Med Rep (Jul 2026)

Intervertebral disc degeneration (IVDD) is increasingly recognized as a systemic collapse of the epigenetic regulatory network, driven by cellular senescence and environmental stressors. The present review provides an overview of the epigenetic regulatory mechanisms governing IVDD, focusing on the dynamic interplay between DNA methylation, histone modifications, N6‑methyladenosine RNA methylation and the non‑coding RNA regulatory triad (microRNAs, long non‑coding RNAs and circular RNAs). The present study evaluates advanced research methodologies (ranging from site‑specific methylation typing and transposase accessible chromatin sequencing to single‑cell multi‑omics and artificial intelligence‑driven predictive modeling) that resolve the spatial and cellular heterogeneities of the degenerating disc niche. Furthermore, the translational constraints of current animal models were critically assessed, advocating for a strategic shift from acute needle‑puncture insults to physiologically relevant aging and genetically engineered progeroid models to better recapitulate human 'epigenetic drift'. Finally, the therapeutic potential of targeted epigenetic editing via CRISPR/dCas9 systems and the development of stimuli‑responsive nanocarriers for precision delivery are highlighted. By bridging methodological innovation with robust model selection, the present review offers a roadmap for transitioning molecular insights into clinical regenerative therapies for spinal health.]]> Wed, 31 Dec 1969 19:00:00 EST 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 Cholangiocyte biology in primary sclerosing cholangitis and other cholangiopathies: pathogenesis, clinical insights, and experimental tools. Jalan-Sakrikar N, Anwar AA, Ali A, Nasser-Ghodsi N, Felzen A, Huebert RC, LaRusso NF, O'Hara SP
Physiol Rev (Jul 2026)

Cholangiocytes are specialized epithelial cells that line the intrahepatic and extrahepatic biliary tree and play a critical role in bile modification, liver homeostasis, and response to injury. Cholangiocytes exhibit notable heterogeneity and plasticity, and their dysfunction is central to a spectrum of diseases targeting the bile ducts, collectively called cholangiopathies. These disorders include genetic, infectious, immune-mediated, and malignant diseases, with primary sclerosing cholangitis (PSC) representing one of the most complex and enigmatic of these disorders. PSC is a progressive, fibro-inflammatory disease of the bile ducts that is closely linked to inflammatory bowel disease, carries a heightened risk of cancer, and lacks any approved therapies. This review explores the biology of cholangiocytes, including their development, functional plasticity, and roles in secretion, absorption, and cellular signaling. We provide a detailed examination of cholangiopathies, particularly PSC, a complex cholangiopathy characterized by a paradoxical state of cholangiocyte senescence and hyperproliferation. We describe how immune cell dysfunction, the gut microbiome, genetic predispositions, and environmental factors converge to mediate PSC pathogenesis. We revisit the foundational technologies that empowered early discoveries and shaped the field as we know it today. We also explore how newer techniques such as organoid cultures, single-cell transcriptomics, epigenomics, and spatialomics have transformed our modern understanding of biliary pathophysiology. Finally, we provide an overview of existing rodent models of cholangiopathies and discuss their relevance to human disease. PSC remains therapeutically unaddressed, and thus ongoing multidisciplinary efforts are essential to developing targeted interventions. This review serves as a comprehensive resource for researchers and clinicians navigating the rapidly evolving landscape of cholangiocyte-centered liver disease research.]]> 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 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 Differential A-to-I editing of SINE B2 RNAs unveils an epitranscriptome response to Aβ neurotoxicity. Mitchell L, Saville L, Gollen B, Haight T, Roy R, Turner C, Cheng Y, Kovalchuk I, Mohajerani MH, Zovoilis A
Life Sci Alliance (Sep 2026)

Adenosine-to-inosine (A-to-I) RNA editing is a major epitranscriptomic mechanism, yet its contribution to non-coding RNA regulation during neurodegeneration is largely unknown. SINE B2 RNAs represent the dominant editing substrates in mice and have been shown to regulate gene expression. Here, we introduce and validate a repeat-aware bioinformatics framework that enables position-specific quantification of A-to-I editing within SINE RNAs, which has been challenging using standard genome-based pipelines. Applying this approach, we identify discrete editing hotspots in mouse SINE B2 RNAs that are selectively increased during early amyloid beta pathology in independent mouse models and in hippocampal neurons exposed to amyloid beta toxicity. Functional perturbation of ADAR activity alters both B2 RNA editing levels and the expression of B2 RNA-regulated genes, directly linking RNA editing to SINE-mediated transcriptional control. Nanopore sequencing confirmed increased RNA modification signals at these regions. Together, our findings establish a previously unrecognized epitranscriptomic response to amyloid beta neurotoxicity mediated by site-specific A-to-I editing of SINE RNAs.]]> Wed, 31 Dec 1969 19:00:00 EST Paternal fenvalerate exposure causes autism-like behavior partly by altering epigenetic reprogramming of the imprinted gene IGF2 in fetal brain and paternal sperm. Qi XM, Shao J, Zhu QL, Deng ZY, Wang T, Chen HR, Xu LH, Li JJ, Wang M, Xu DX, Wang B, Meng XH
Ecotoxicol Environ Saf (Jul 2026)

Fenvalerate, a representative type II pyrethroid insecticide, is well established in the literature. Fenvalerate exerts developmental and neurological toxicity. We assessed whether paternal fenvalerate exposure induces autism-like behavioral alterations in offspring using a mouse model. Behavioral tests, including the three-chamber social interaction, self-grooming, and marble-burying tests, showed altered social and repetitive behaviors in offspring from fenvalerate-exposed fathers. NeuN, a mature neuronal marker, was reduced in the medial prefrontal cortex (mPFC) of weaning offspring from paternal fenvalerate-exposed groups. Nissl staining showed that the number of surviving neurons is reduced in the mPFC of weaning pups with paternal exposure to fenvalerate. Nestin, a marker for neural stem cells, was decreased in the fetal forebrain from paternal fenvalerate-exposed groups. Transcriptome analysis and RT-PCR showed that insulin-like growth factor 2 (IGF2), a neurotrophic factor, was downregulated in the paternal fenvalerate-exposed group. IGF2 protein was reduced in the fetal forebrain from paternal fenvalerate-exposed group. In addition, paternal fenvalerate exposure reduced methylation of the IGF2 imprinted control region (ICR) in fetal forebrain and paternal sperm. In conclusion, autism-like behaviors appear in offspring after paternal exposure to fenvalerate, which may partly be related to disruptions in epigenetic reprogramming of IGF2 in the developing brain and paternal sperm.]]> Wed, 31 Dec 1969 19:00:00 EST Integrative MeRIP-seq and RNA-seq analysis reveals mA-mediated epigenetic regulation of host-virus interactions during HSV-2 infection. Li J, Lin D, Xie J, Zhang Z, Qian Y, Xu S, Xu J, Hu Y, Shi J
Virology (Sep 2026)

Herpes simplex virus type 2 (HSV-2), a highly prevalent pathogen responsible for genital herpes, is characterized by neurotropism and the ability to establish lifelong latent infection. N6-methyladenosine (mA) is a widespread epitranscriptomic modification that plays a critical role in regulating RNA metabolism and gene expression. In this study, we used methylated RNA immunoprecipitation sequencing (MeRIP-seq) and RNA sequencing (RNA-seq) to profile mA modifications and transcriptomic changes in human foreskin fibroblasts (HFF-1) infected with HSV-2. We identified 9477 common mA peaks and 15,842 differentially methylated peaks, with a predominant localization within coding sequences. Analysis of mA modification sites on HSV-2 gene transcripts from MeRIP-seq data identified a total of 145 mA sites across 63 viral genes. Functional enrichment analysis revealed that differentially mA-modified genes are involved in key biological processes, including gene expression, neural signaling, and immune responses. Pathway analysis highlighted significant enrichment in the NOD-like receptor signaling pathway, Rap1 signaling, endocytosis, and adherens junction pathways. RNA-seq analysis identified 6172 differentially expressed genes, of which 3181 were upregulated and 2991 were downregulated. Integrative analysis of the two datasets revealed that genes exhibiting both altered mA methylation and differential expression were significantly enriched in pathways including TNF signaling and the NOD-like receptor pathway. This study provides the first comprehensive landscape of mA epitranscriptomic modifications and their association with transcriptomic reprogramming during HSV-2 infection, offering new insights into the epigenetic mechanisms of virus-host interactions.]]> Wed, 31 Dec 1969 19:00:00 EST N6-methyladenosine modification in the context of viral infection: from molecular mechanism to therapeutic potential. Wu X, Deng Z, Li Y, Shi C
Virus Res (Jul 2026)

N-methyladenosine (mA) is the most abundant and dynamically regulated RNA modification in eukaryotic cells, which modulates key RNA metabolic processes including splicing, stability, nuclear export, degradation and translation. During viral infection, mA exerts a pivotal regulatory role by modifying both viral RNAs and host cellular transcripts. Accumulating evidence demonstrates that viruses hijack the host mA machinery through diverse mechanisms to reprogram the host epitranscriptome, in favor of viral replication. Targeting the host mA machinery has emerged as a promising novel antiviral therapeutic strategy. This review focuses on the molecular mechanisms underlying viral hijacking of host mA modifications and explores the therapeutic potential of targeting the viral hijacking mechanisms of the host mA machinery.]]> Wed, 31 Dec 1969 19:00:00 EST mA-Mediated epitranscriptomic control of mitochondrial dysfunction in neurodegeneration. Jauhari A
Mitochondrion (Sep 2026)

Mitochondrial dysfunction is a common pathology of neurodegenerative diseases, which contributes to neuronal vulnerability via excessive oxidative stress, impaired bioenergetics, and dysregulated apoptosis. Emerging studies highlighted the critical role of epitranscriptomic RNA modifications, particularly N-methyladenosine (mA), in mitochondrial gene expression regulation and cellular stress responses. mA modifications are installed by methyltransferases ("writers," METTL3/METTL14), recognized by reader proteins (YTH domain family proteins, IGF2BPs), and removed by demethylases ("erasers," FTO, ALKBH5), collectively orchestrating mRNA splicing, localization, stability, and translation. Recent evidence demonstrates that mA modifications modulate both nuclear-encoded and mitochondrially encoded transcripts and regulate key mitochondrial processes, including fission/fusion dynamics, oxidative phosphorylation, mitophagy, and apoptosis. Dysregulation of mA machinery disrupts mitochondrial homeostasis, exacerbates oxidative stress and neuroinflammation, and promotes neuronal loss. Importantly, pharmacological or genetic modulation of mA regulators can restore mitochondrial function, inhibit caspase activation, and dampen pro-inflammatory signaling, underscoring their therapeutic potential. This review consolidates current insights into mitochondrial epitranscriptomics, emphasizing how mA modifications act as central regulators of mitochondrial stress responses and neurodegeneration.]]> Wed, 31 Dec 1969 19:00:00 EST NAT10-dependent ac4C mRNA modification programs fibroblast pathogenicity in systemic sclerosis. Tang W, Xu Y, Liu W, Wang W, Jiang C, Yi X, Jiang M, Wang N, He S, He J, Shen J, Cong W, Zhu Z
Pharmacol Res (Jul 2026)

Systemic sclerosis (SSc) is characterized by progressive fibrosis driven by persistent activation of dermal fibroblasts, yet the epigenetic and epitranscriptomic mechanisms sustaining fibroblast pathogenicity remain incompletely defined. Here, we investigated the role of N-acetyltransferase 10 (NAT10)-mediated N4-acetylcytidine (ac4C) RNA modification in fibroblast activation and fibrotic remodeling. Integrative analyses of single-cell transcriptomics, human SSc skin, in vitro assays, in vivo models, and fibroblast-specific knockout mice revealed that NAT10 is upregulated in pathogenic fibroblast populations and contributes to fibrotic progression. Genetic ablation or pharmacological inhibition of NAT10 attenuated fibroblast proliferation and extracellular matrix deposition across experimental systems. Multi-omics analyses identified COL11A1 and ZNF621 as downstream targets associated with NAT10, with site-specific ac4C modifications detected on both transcripts. Mechanistically, NAT10-dependent ac4C deposition was associated with increased mRNA stability and transcriptional output of these pro-fibrotic genes. Notably, suppression of ZNF621 partially reversed the pro-fibrotic phenotypes induced by NAT10 overexpression, supporting its functional relevance downstream. Together, these findings define an epitranscriptomic mechanism contributing to fibroblast activation in SSc and suggest that targeting the NAT10-ac4C axis may represent a potential therapeutic strategy for fibrotic disease.]]> Wed, 31 Dec 1969 19:00:00 EST RNA methylation in kidney disorders: Insights into molecular machinery and therapeutic opportunities. Li Z, Chen Y, Zhang X, Lv J, Chen J, Chen D, Yao Q
Cell Signal (Sep 2026)

Kidney disorders, including acute kidney injury (AKI), chronic kidney disease (CKD), diabetic nephropathy (DN), and clear cell renal cell carcinoma (ccRCC), represent major causes of morbidity and mortality worldwide and remain significant challenges in clinical management because of their complex pathogenesis and limited therapeutic options. Recent advances in epitranscriptomics have highlighted RNA methylation as an important post-transcriptional regulatory mechanism involved in renal physiology and disease development. Diverse RNA modifications, including N6-methyladenosine (m6A), 5-methylcytosine (m5C), N1-methyladenosine (m1A), N7-methylguanosine (m7G), and 3-methylcytidine (m3C), dynamically regulate RNA metabolism by affecting transcript stability, translation, splicing, and degradation. Increasing evidence demonstrates that RNA methylation regulators, including methyltransferases such as METTL3 and METTL14, demethylases such as FTO and ALKBH5, and reader proteins such as YTH domain-containing family members, participate in multiple pathogenic processes, including inflammation, fibrosis, oxidative stress, metabolic dysregulation, and tumor progression in renal disorders. Aberrant expression of these regulators has been closely associated with disease severity and progression. In this review, we summarize current knowledge regarding major RNA methylation modifications and their regulatory machinery in a spectrum of kidney diseases, with particular emphasis on the molecular mechanisms through which RNA methylation influences renal injury and repair. We further discuss the emerging value of RNA methylation-related molecules as potential biomarkers and therapeutic targets, aiming to provide new insights into epitranscriptomic regulation in kidney disease and its translational potential.]]> Wed, 31 Dec 1969 19:00:00 EST Screening of M6a methylated genes associated with preovulatory follicle development in Bashang long-tailed chicken. Duan X, Xie J, Yin S, Zhang L, Liu Y
Poult Sci (Jul 2026)

N6-methyladenosine (m6A) methylation, a pivotal post-transcriptional modification, regulates RNA metabolism and biological processes, including reproduction. However, its role in poultry follicular development remains unclear. This study integrated MeRIP-seq and RNA-seq analyses to profile m6A modifications and gene expression in preovulatory follicles of Bashang Long-tailed chickens. We identified 14,024 m6A peaks in small yellow follicles(SYF) and 14,063 in small white follicles(SWF) . A total of 651 differential m6A peaks (DMPs), with 562 upregulated and 89 downregulated in SWF compared to SYF were identified. Transcriptome analysis identified 3,250 differentially expressed genes (DEGs), including 319 upregulated and 2,931 downregulated in SWF. Integrated multi-omics analysis identified 95 genes with concurrent m6A and expression changes, of which MAP1LC3C were identified as target of post-transcriptional m6A regulation. We then constructed the regulation network of MAP1LC3C gene in pre-ovulatory follicle development of chickens. These findings provide insights into epigenetic mechanisms underlying avian reproduction, offering potential targets for improving egg production in native breeds of China.]]> Wed, 31 Dec 1969 19:00:00 EST Neuronutrition in ASD: Involvement of gut microbiota, oxidative stress and inflammatory markers. Avolio E, Olivito I, Minervini D, Soda T, De Bartolo A, Rocca C, Alò R, Facciolo RM
Neurosci Biobehav Rev (Aug 2026)

Autism spectrum disorder (ASD) is a neurodevelopmental disorder displaying altered human behaviors, such as social interaction impairments, stereotypical/repetitive activities and emotional dysregulation. Children with ASD are often affected by gastrointestinal problems and gut microbiota dysbiosis. Inflammation and immune dysfunction are key contributors to ASD, as shown by high proinflammatory cytokines and oxidative stress. Indeed, notable implication of the nuclear factor kappa B in the severity of ASD derives from its ability to amplify neuroinflammation. This narrative review focused attention on neuronutrition and gut microbiota manipulation for mitigation of ASD symptoms, including neuroinflammation and oxidative stress. Studies in both rodents and humans with ASD have revealed that both pure and mixed Lactobacillus and Bifidobacterium were effective in ameliorating behavioral symptoms and GABA/glutamate imbalance. Often, the combined use of probiotics and prebiotics can have greater health benefits in ASD. Additionally, dietary interventions and microbiota transfer therapies along with low-to-moderate-intensity exercise have been proposed to improve gastrointestinal and behavioral symptoms. However, despite some encouraging results, biases in the neuronutrition/microbiota literature still exist. Indeed, many studies rely on small sample sizes, cross-sectional designs, and heterogeneous populations that differ in diet, medications, and comorbidities. In this context, the development of a precision diet tailored to individual gut microbiome profiles will allow for a broader understanding of the microbial ecosystem and relative therapeutical applications. Hence, by integrating metagenomics, metabolomics, epigenomics, with evaluation of environmental and nutritional factors, it will be possible to significantly improve the quality of life for people with ASD and their families.]]> Wed, 31 Dec 1969 19:00:00 EST The transformative role of single-cell analysis in multifactorial disorders research. Wang CY, Ko CC, Kumar S, Xuan DTM, Lin HR, Lee YK, Nguyen NUN, Yang PM, Solomon DD
Methods (Jul 2026)

Multifactorial inherited disorders (MIDs) arise from complex interactions between polygenic risk and environmental exposures, presenting major challenges for mechanistic discovery, patient stratification, and targeted therapy development. While traditional approaches like genome-wide association studies (GWAS) and bulk omics profiling have identified broad associations, they often struggle to resolve the cellular context in which these interactions drive pathogenesis.Emergingsingle-cell technologies now offer unprecedented resolution to dissect tissue heterogeneity, define rare or transient disease-relevant cell states, and map dynamic trajectories across tissues and disease stages. This reviewprovides a comprehensive synthesis ofcurrent single-cell methodologies including transcriptomic, epigenomic, proteomic, and spatial techniques and their application to MID research. We explore how these toolsare revealingcell-type-specific regulatory circuits,contextualizingthe functional impact of inherited risk variants, andelucidatingcellular responses to environmental perturbations.We propose thatintegrating single-cell multi-omics data is critical for illuminating the mechanistic basis of complex traits and for advancing biomarker discovery. However, significant challenges remain, including technical variability, limited cohort scalability, difficulties in multi-modal data integration, and a lack of standardized analytical workflows for polygenic diseases. Overcoming these barriers will require harmonized study designs, robust computational frameworks, and the incorporation of longitudinal and environmental exposure data.Ultimately, we conclude thatsingle-cell analysis is poised to transform MID research, offering a powerful new paradigm for mechanistic insight, therapeutic innovation, and the realization of precision medicine.]]> Wed, 31 Dec 1969 19:00:00 EST