'; ?> 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 Sat, 13 Dec 2025 23:14:14 EST Sat, 13 Dec 2025 23:14:14 EST jirtle@radonc.duke.edu james001@jirtle.com Assessing the impact of bariatric surgery on cardiovascular risk in type 2 diabetes: a systematic review and meta-analysis using OMICs data. Almazrouei B, Mousa M, Al Dain Marzouka N, Barajas-Gamboa JS, Abril C, Al Safar H
Diabetol Metab Syndr (Dec 2025)

Type 2 diabetes (T2D) is a complex, multifactorial metabolic disorder, and while bariatric surgery has emerged as a promising intervention for obesity-related T2D with significant metabolic benefits, its long-term durability and potential for remission vary among patients. This systematic review and meta-analysis explore how omics modalities-such as genomics, epigenomics, transcriptomics, metabolomics, proteomics, and gut microbiome-can reveal potential biomarkers linked to cardiovascular disease (CVD) of T2D patients who undergo bariatric surgery. Following PRISMA 2020 guidelines, a systematic search in PubMed identified 49 eligible studies. The meta-analysis of eight proteomic biomarkers, showed significant post-surgery improvements in total cholesterol (mean difference (MD) 0.44 (95% CI: 0.06-0.82), p = 0.02), triglycerides (MD 1.00 (0.77-1.24), p < 0.00001), LDL cholesterol (MD 0.27 (0.02, 0.52), p = 0.03), HDL cholesterol (MD -0.22 (-0.30, -0.15), p < 0.00001), hsCRP (MD 0.64 (0.44, 0.84), p < 0.00001), C peptide levels (MD 1.29 (0.96, 1.61), p < 0.0001), and IL-6 (MD 1.84 (0.85, 2.84), p = 0.0003). These findings highlight the value of integrated omics in developing personalized diagnostics, predicting disease risks, and designing targeted therapies. The present study is the first systematic review presenting the omics disciplines that offer a comprehensive view of the effectiveness of bariatric surgery in managing T2D, subsequently reducing the risk of CVD.]]> Wed, 31 Dec 1969 19:00:00 EST Regions of Homozygosity Identified with a Chromosomal Microarray in a Korean Population: Distribution, Frequency, and Clinical Interpretation. Kim J, Min S, Seol CA, Seo EJ
Ann Lab Med (Jan 2026)

Single nucleotide polymorphism-based chromosomal microarray analysis (CMA) can detect regions of homozygosity (ROHs), which may be associated with medical conditions; however, limited ROH data, especially in East Asians, complicates clinical interpretations. We characterized ROH distributions and frequencies in a Korean population using CMA, highlighting clinically relevant findings, including suspected uniparental disomy (UPD), using standardized criteria.]]> Wed, 31 Dec 1969 19:00:00 EST A hitchhiker's guide to single-cell epigenomics: Methods and applications for cancer research. Moreno-Gonzalez M, Sierra I, Kind J
Int J Cancer (Jan 2026)

Genetic mutations are well known to influence tumorigenesis, tumor progression, treatment response and relapse, but the role of epigenetic variation in cancer progression is still largely unexplored. The lack of epigenetic understanding in cancer evolution is in part due to the limited availability of methods to examine such a heterogeneous disease. However, in the last decade the development of several single-cell methods to profile diverse chromatin features (chromatin accessibility, histone modifications, DNA methylation, etc.) has propelled the study of cancer epigenomics. In this review, we detail the current landscape of single-omic and multi-omic single-cell methods with a particular focus on the examination of histone modifications. Furthermore, we provide recommendations on both the application of these methods to cancer research and how to perform initial computational analyses. Together, this review serves as a referential framework for incorporating single-cell methods as an important tool for tumor biology.]]> Wed, 31 Dec 1969 19:00:00 EST Single-Cell Multi-Omics Sequencing Technologies and Their Applications in Livestock and Poultry Research. Cao J, Zhou X, Liu J, Liu D, Liu G
J Agric Food Chem (Dec 2025)

Single-cell multiomics technologies enable the detailed resolution of cellular heterogeneity by integrating multidimensional information─including genomics, epigenomics, transcriptomics, and proteomics─at the single-cell level to construct high-resolution molecular maps. Compared with conventional bulk sequencing methods, these technologies overcome the limitations of signal averaging, allowing for the identification of rare yet functionally critical cell subpopulations that would otherwise remain obscured. In livestock and poultry research, single-cell multiomics offers a novel approach to dissect the biological basis of key economic traits such as reproduction, growth, meat production, and disease resistance, demonstrating immense potential for elucidating the molecular mechanisms underlying desirable phenotypes. This review systematically outlines the developmental trajectory and core principles of single-cell multiomics sequencing technologies. We summarize their major applications in fundamental livestock and poultry research and discuss current challenges and future opportunities in the field. Our aim is to provide a comprehensive reference to guide future research in animal science.]]> Wed, 31 Dec 1969 19:00:00 EST From genes to lifestyle: A multi-dimensional framework for Alzheimer's disease prevention and therapy. Su L, Wang Y
Ageing Res Rev (Jan 2026)

Alzheimer's disease (AD) is a complex neurodegenerative disorder driven by multilayered molecular and cellular mechanisms that cannot be fully elucidated through single-omics approaches. Consequently, large-scale multi-omics integration-encompassing transcriptomics, epigenomics (e.g., methylation), and genetic association studies (GWAS/eQTL/mQTL)-has uncovered critical genetic and epigenetic networks underlying disease risk and progression.Based on these integrative insights, this review emphasized several genes-including KLHL21, SCN2B, ZNF415, and PITRM1-as potential contributors to AD pathogenesis. Notably, single-cell and spatial transcriptomics analyses revealed specific enrichment of these genes in astrocytes, underscoring the pivotal role of this cell type in Aβ clearance, tau propagation, and neuroinflammation. Exercise interventions were shown to selectively modulate the expression of these genes, providing molecular support for the preventive and therapeutic potential of non-pharmacological lifestyle strategies. Drug repurposing analyses using DrugBank have identified promising therapeutic candidates, including FDA-approved agents (e.g., valproic acid, raloxifene, and clomipramine) and naturally derived compounds (e.g., quercetin and fisetin), which may modulate key AD-related pathways. Furthermore, emerging evidence of miRNA-gene regulatory networks suggested an additional layer of post-transcriptional control that may regulate responses to pathological stimuli. Collectively, these integrative insights advocated for a multidimensional precision medicine framework that spans genetic, cellular,network, and lifestyle levels of regulation. This shift from single-target therapeutics to an integrated "gene-cell-network-lifestyle" paradigm open new theoretical and translational avenues for delaying or mitigating AD progression.]]> Wed, 31 Dec 1969 19:00:00 EST Integrative Multi-Adaptive Biological-Mental-Social Network Modeling of Changing Social and Organizational Contexts, Epigenetics, Personality Traits and Burnout Dimensions. Bouma D, Treur J, Hendrikse SCF
Int J Neural Syst (Dec 2025)

This research addresses the interplay of changing social and organizational context factors with the big five personality traits and the three main characterizing elements of burnout. A computational analysis is contributed based on an integrative biological-mental-social network modeling approach. The simulation results show how two people who are high in personality traits such as agreeableness, openness, extraversion, conscientiousness, and highly sensitive to neuroticism, are vulnerable to reaching a burnout level in all dimensions whenever the organizational context is changing in a less favorable direction. By a What-If analysis, it is analyzed how important characteristics affect the outcomes and indicate how, in a qualitative sense, that is in line with empirical literature. Several differentiations are made. In particular, the connection between the three dimensions of burnout shows that it is possible that one employee reaches a burnout state while the other does not. It is also shown how therapy alone may not be sufficient as a long-term treatment, but therapy of one employee does affect the other. As numerical data are not (yet) available, further numerical validation has been proposed for future work.]]> Wed, 31 Dec 1969 19:00:00 EST [Expression of Concern] Gene therapy for human colorectal cancer cell lines with recombinant adenovirus 5 based on loss of the insulin‑like growth factor 2 imprinting. Sun H, Pan Y, He B, Deng Q, Li R, Xu Y, Chen J, Gao T, Ying H, Wang F, Liu X, Wang S
Int J Oncol (Jan 2026)

Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that, for the immunohistochemical data shown in Fig. 2B and C, the PBS/TUNEL panel in Fig. 2B appeared to be strikingly similar to the PBS/E1A panel shown in Fig. 2C. Furthermore, for the E1A experiments portrayed in Fig. 2C, portions of the data panels shown for the H101 and E1A groups also appeared to be strikingly similar, albeit with rotation of one of the panels. The authors were contacted by the Editorial Office to offer an explanation for this possible anomaly in the presentation of the data in this paper, although up to this time, no response from them has been forthcoming. Owing to the fact that the Editorial Office has been made aware of potential issues surrounding the scientific integrity of this paper, we are issuing an Expression of Concern to notify readers of this potential problem while the Editorial Office continues to investigate this matter further. [International Journal of Oncology 46: 1759‑1767, 2015; DOI: 10.3892/ijo.2015.2852].]]> Wed, 31 Dec 1969 19:00:00 EST Twin pairs discordant for incident coronary artery disease reveal epigenetic and transcriptomic differences by gene region. Skovgaard AC, Thinggaard M, Hjelmborg JV, Nejad AM, Beck HC, Tan Q, Soerensen M
Mol Genet Genomics (Dec 2025)

Cardiovascular diseases are the leading causes of mortality globally, of which coronary artery disease (CAD) is the most frequent. Several epigenomics and transcriptomics studies of CAD have been conducted, however, only a few studies have utilized the statically powerful discordant twin pair design, which reduces the confounding introduced by genetics. Finally, no study has investigated the link between the DNA methylation position and gene expression levels. The present study aims at filling this knowledge gap, to present novel biomarkers of CAD. We investigated 44 Danish twin pairs that were discordant for incident CAD, for whom, both genome-wide DNA methylation (CpG) and gene expression (probe) data were available. We identified CpGs and probes, which were more different within the twin pairs than expected by change, and investigated these by Cox regression analysis. CpGs and probes belonging to the same gene were divided into groups based on their directions of effect, and these genes were investigated by gene set enrichment and interaction network analyses. Overall, we found that CAD co-twins showed DNA methylation patterns leading to up-regulated gene expression; especially with demethylation of promoters and methylation of gene bodies, compared to their non-CAD co-twin. Generally, we found that the largest biological group of up-regulated pathways related to immune-inflammation processes, whereas down-regulated pathways related to muscle system biology, among others. Hence, the present study uncovers a specific pattern between DNA methylation position and gene expression levels relating to CAD, pointing to a need for additional studies. However, such multi-omics designs are surprisingly rare.]]> Wed, 31 Dec 1969 19:00:00 EST Multiomics Insights into Epigenetic Mechanisms and Their Role as Biomarkers for Acute Coronary Syndrome. D'Agostino A, Rosalinda M, Salvatore M, Monica F
Heart Fail Clin (Jan 2026)

Acute coronary syndrome (ACS) is a complex cardiovascular condition driven by chronic inflammation, immune system imbalances, and epigenetic alterations. Recent research highlights the crucial role of epigenetic modifications in disease progression. Furthermore, differentially methylated regions influence expression in genes associated with immune signaling and cellular functions in ACS patients. ACS is a multifactorial disease driven by complex interactions between genetic, epigenetic, and environmental factors. By leveraging multiomics approaches, clinicians and researchers can uncover novel pathophysiological mechanisms and refine therapeutic strategies for improved cardiovascular outcomes in ACS patients. Integrating multiomics technologies with machine learning-driven analysis is revolutionizing our understanding of ACS.]]> Wed, 31 Dec 1969 19:00:00 EST Epigenomics-guided precision oncology: Chromatin variants in prostate tumor evolution. Furlano K, Keshavarzian T, Biernath N, Fendler A, de Santis M, Weischenfeldt J, Lupien M
Int J Cancer (Jan 2026)

Prostate cancer is a common malignancy that in 5%-30% leads to treatment-resistant and highly aggressive disease. Metastasis-potential and treatment-resistance is thought to rely on increased plasticity of the cancer cells-a mechanism whereby cancer cells alter their identity to adapt to changing environments or therapeutic pressures to create cellular heterogeneity. To understand the molecular basis of this plasticity, genomic studies have uncovered genetic variants to capture clonal heterogeneity of primary tumors and metastases. As cellular plasticity is largely driven by non-genetic events, complementary studies in cancer epigenomics are now being conducted to identify chromatin variants. These variants, defined as genomic loci in cancer cells that show changes in chromatin state due to the loss or gain of epigenomic marks, inclusive of histone post-translational modifications, DNA methylation and histone variants, are considered the fundamental units of epigenomic heterogeneity. In prostate cancer chromatin variants hold the promise of guiding the new era of precision oncology. In this review, we explore the role of epigenomic heterogeneity in prostate cancer, focusing on how chromatin variants contribute to tumor evolution and therapy resistance. We therefore discuss their impact on cellular plasticity and stochastic events, highlighting the value of single-cell sequencing and liquid biopsy epigenomic assays to uncover new therapeutic targets and biomarkers. Ultimately, this review aims to support a new era of precision oncology, utilizing insights from epigenomics to improve prostate cancer patient outcomes.]]> Wed, 31 Dec 1969 19:00:00 EST From renal development to pathology: An analysis of the multilevel role of insulin‑like growth factor 2 (Review). Sun Y, Hao W, Liu W, Hu W
Mol Med Rep (Jan 2026)

Insulin‑like growth factor 2 (IGF2) is a multifunctional polypeptide hormone that serves important roles in embryonic development, metabolic regulation and disease pathogenesis. IGF2 expression is tightly regulated by genomic imprinting, which restricts transcription to the paternal allele. IGF2 modulates cellular processes, including proliferation, differentiation and metabolic homeostasis, by activating downstream signaling cascades via binding to IGF1 receptor, insulin receptor isoform A and IGF2 receptor. IGF2 is important for kidney development, promoting both nephron formation, and the functional maintenance of renal tubules and glomeruli. Aberrant IGF2 expression is associated with the pathogenesis of diverse renal diseases, including acute kidney injury, chronic kidney disease, diabetic nephropathy, renal cell carcinoma and Wilms' tumor. Under pathological conditions, IGF2 promotes renal fibrosis and promotes tumor expansion and progression by activating key signaling pathways such as the PI3K/Akt and TGF‑β pathways. Due to these roles, IGF2 has attracted growing clinical interest as a potential therapeutic target. The present review presents a comprehensive analysis of the structure and function of IGF2, its roles in renal pathophysiology, and its therapeutic potential, while outlining future research directions.]]> Wed, 31 Dec 1969 19:00:00 EST Integration of omics data in the diagnosis and therapy of glioblastoma. Möller C, Schoof M, Ligon KL, Schüller U
Brain Pathol (Jan 2026)

Since the 2016 update of the WHO Classification of Tumors of the Central Nervous System, omics data have been officially integrated into the diagnostic process for glioblastoma, the most prevalent and aggressive primary malignant brain tumor in adults. This review will examine the current and future integration of omics data in both the diagnosis and therapy of glioblastomas. The current clinical use of omics data primarily focuses on genomics for determining the IDH- and H3-wildtype status of the tumor, and on epigenomics, such as assessing MGMT promoter methylation status as a prognostic and predictive biomarker. However, it can be anticipated that the usage and importance of omics data will likely increase in the future. This work highlights how omics technologies have significantly enhanced our understanding of glioblastoma, particularly of its extensive heterogeneity. This enhanced understanding has not only improved diagnostic accuracy but has also facilitated the identification of new predictive and/or prognostic biomarkers. It is likely that the ongoing integration of omics data will transform many aspects of the diagnostic process, including sample acquisition. Additionally, omics data will be integrated into future glioblastoma treatment procedures, with possible applications ranging from identifying potential therapeutic targets to selecting individual treatment plans. The implications of the ongoing integration of omics data for clinical routine, future classification systems, and trial design are also discussed in this review, outlining the pivotal role omics data play in shaping future glioblastoma diagnosis and treatment.]]> Wed, 31 Dec 1969 19:00:00 EST Decoding preterm birth: Non-Invasive biomarkers and personalized multi-omics strategies. Farzizadeh N, Najmi Z, Rosenbaum AJ, Amoozgar M, Hariri A, Aminbeidokhti M, Khosravi A, Zarrabi A
Dev Biol (Jan 2026)

A birth that occurs prior to 37 weeks of gestation is referred to as preterm birth (PTB). PTB is a health concern globally with significant outcomes including neonatal morbidity and mortality. Advancements in multi-omics have revolutionized the understanding of PTB pathogenesis, offering new opportunities for early prediction and risk categorization. This review highlights emerging liquid biomarkers derived from proteomic, metabolomic, genomic, transcriptomic, and epigenomic studies, emphasizing the integrative power of multi-omics approaches. Proteomic analyses have revealed key proteins in maternal and fetal compartments associated with inflammatory and extracellular matrix pathways, while metabolomics have identified lipid and metabolite profiles linked to energy metabolism and fetal development. Genomic and epigenomic studies have uncovered genetic variations and microRNAs involved in uterine contractility and immune modulation, providing novel insights into PTB's molecular underpinnings. Transcriptomic research further underscores the act of long non-coding RNAs (ncRNAs) in regulating gene expression and inflammatory responses. Multi-omics integration, coupled with machine learning models, has demonstrated superior predictive accuracy by synthesizing data across these domains, revealing intricate molecular interactions underlying PTB. Future research should prioritize longitudinal multi-omics studies to capture dynamic biological changes during pregnancy, expanding diverse population cohorts to enhance generalizability. Translating multi-omics insights into clinical practice necessitates collaborative efforts to develop cost-effective, accessible biomarker panels and establish standardized guidelines for implementation. These advancements hold the potential to transform prenatal care through personalized risk assessment and targeted preventive strategies, reducing the global burden of PTB.]]> Wed, 31 Dec 1969 19:00:00 EST Single-cell multi-omics characterize colorectal tumors, adjacent healthy tissue and matched (tumor) organoids identifying CRC-unique features. Yu Z, Derksen M, Te Pas BM, Ladstätter S, Overmeer R, Brazda P, van de Wetering M, Pourfarzad F, Vries RGJ, Megchelenbrink W, Bock C, Altucci L, Stunnenberg HG
Int J Cancer (Dec 2025)

Colorectal cancer (CRC) arises in the colorectal tissue driven by genetic disorder or the accumulation of somatic mutations, leading to abnormal epithelial cell growth. In this study, we employed single-nucleus multi-omics analysis, including single-nucleus RNA-seq and single-nucleus ATAC-seq, on over 100,000 high-quality nuclei to investigate the molecular landscape of both primary tissue and patient-derived organoids (PDOs). Our analysis showed that normal PDOs (N-PDOs) derived from tissue adjacent to tumors replicate the cellular composition and differentiation trajectory of colorectal crypts. In contrast, tumor PDOs (T-PDOs) showed patient-specific transcriptomic and epigenomic heterogeneity yet consistently maintained a stem cell-like state. T-PDOs retained the somatic mutation profile of the primary tumor while also exhibiting de novo mutations not detected in either the primary tumor or N-PDOs. Notably, inferred cell-cell interaction analysis highlighted the activin signaling pathway as a potential unique feature of fibroblast-epithelial interactions within the tumor microenvironment. This study provides a comprehensive view of the transition from normal to malignant colorectal epithelium and underscores the utility of PDOs as a faithful model for capturing both conserved and patient-specific features of colorectal cancer.]]> Wed, 31 Dec 1969 19:00:00 EST DNA methylation of genes involved in lipid metabolism drives adiponectin levels and metabolic disease. Sinke L, Delerue T, Wilson R, Lu X, Xia Y, Costeira R, Nasr MK, Beekman M, Franke L, Zhernakova A, Fu J, Gieger C, Herder C, Koenig W, Peters A, Ordovas JM, Dörr M, Grabe HJ, Nauck M, Bell JT, Teumer A, Snieder H, Waldenberger M, Slagboom PE, Heijmans BT
Diabetologia (Jan 2026)

Despite playing critical roles in the pathophysiology of type 2 diabetes and other metabolic disorders, the molecular mechanisms underlying circulating adipokine levels remain poorly understood. By identifying genomic regions involved in the regulation of adipokine levels and adipokine-mediated disease risk, we can improve our understanding of type 2 diabetes pathogenesis and inter-individual differences in metabolic risk.]]> Wed, 31 Dec 1969 19:00:00 EST Nap1L4a Cooperates with Scl/Klf1 to Recruit H2A.Z in Mediating Interactions Among Cis-Regulatory Elements and Transcription Required for Primitive Erythropoiesis in Zebrafish. Shi J, Lai F, Shen Z, Zhang X, Wang H, Liu W, Wang Y, Li K, Li G, Fang Y, Liu JX
Adv Sci (Weinh) (Dec 2025)

The chromatin remodeler nucleosome assembly protein 1-like 4 (Nap1L4) is highly expressed in megakaryocyte-erythroid progenitors (MEPs) and erythroid cells. Mutations, deletions, and aberrant expressions of Nap1L4 are observed in diseases such as acute myeloid leukemia (AML). However, the roles of Nap1l4a in erythropoiesis and related diseases, as well as the underlying mechanisms, remain unknown. Here, it is demonstrated that zebrafish nap1l4a homozygous mutants (nap1l4a) are more sensitive to hypoxia stress during the early embryonic stage and exhibit impaired primitive erythropoiesis. Mechanistically, zebrafish Nap1l4a interacts with the erythropoietic transcription factors (TFs) Scl and Klf1, and recruits the histone variant H2A.Z. This interaction remodels the cis-regulatory element (CRE) landscape and promotes nascent RNA transcription of erythropoietic genes. Meanwhile, Nap1l4a deficiency impairs chromatin accessibility at the epigenetic regulators kdm6b and kmt2c. This results in expanded H3K27me3 and diminished H3K4me1 in erythrocytes, leading to altered histone landscapes at erythropoiesis TF loci and reduced TF expression. Moreover, Nap1l4a regulates primitive erythropoiesis by transcriptionally and epigenetically modulating the canonical WNT/β-Catenin pathway. Together, the findings reveal a lineage-selective transcription, with histone epigenomics-dependent role for nap1l4a in vertebrate primitive erythropoiesis. These findings highlight potential mechanisms underlying human blood disorders and hypoxia responses associated with Nap1l4a deficiency.]]> Wed, 31 Dec 1969 19:00:00 EST Immunofluorescence Staining and Microscopic Imaging of Plant Nuclei for Epigenetic Modifications. Gandhivel VH, Raju S, Shivaprasad PV
Methods Mol Biol (2026)

Histone posttranslational modifications (PTMs) and DNA methylation are the predominant epigenetic modifications on the chromatin that regulate gene expression. These modifications can be spatially resolved using microscopic examination of the nuclei with the help of commercially available antibodies. Here, we describe a detailed method to obtain intact nuclei from plant tissues and reproducibly immunostain the nuclei for specific chromatin marks and microscopic examination. This method can be readily extended to multiple plant species as the antibodies are raised against conserved epigenetic marks.]]> Wed, 31 Dec 1969 19:00:00 EST Multiomics Data Synthesis of FAM83H in Amelogenesis Imperfecta. Leban T, Kunej T
Int Dent J (Dec 2025)

FAM83H is a critical gene implicated in amelogenesis imperfecta type IIIA (AI type IIIA), but its precise role in enamel formation remains poorly understood. Fragmented datasets, inconsistent terminology, and limited integrative analyses hinder functional interpretation. This study presents a comprehensive multi-omics analysis of FAM83H-associated AI type IIIA.]]> Wed, 31 Dec 1969 19:00:00 EST Using Epigenetic Data to Deconvolute Immune Cells in Cancer from Blood Samples. Boughanem H, Ouzounis S, Callari M, Sanz-Pamplona R, Macias-Gonzalez M, Katsila T
Methods Mol Biol (2026)

DNA methylation plays a crucial role in regulating gene expression and is a hallmark of epigenetic dysregulation in human tumors. High-throughput DNA methylation profiling can unravel intricate patterns in cancer. Moreover, understanding immune cell dynamics is essential for comprehending cancer progression and treatment response. Using DNA methylation data in immune cells, we can apply deconvolution algorithms estimate proportions of major immune cell types, providing insights into immune status and its implications in cancer. Functional analysis can identify specific overrepresented or underrepresented immune cell subsets, potentially uncovering novel biomarkers or therapeutic targets. This pipeline presents a detailed workflow in RStudio for DNA methylation studies and immune cell deconvolution, enhancing reproducibility and efficiency. The workflow integrates preprocessing, analysis, and visualization steps, facilitating robust inference of cell-type proportions from DNA methylation data.]]> Wed, 31 Dec 1969 19:00:00 EST Protein restriction reprograms the multi-organ proteomic landscape of mouse aging. Lu T, Xie Y, Wang Y, Lin X, Cai X, Zhang Y, Nie Z, Su C, Gou W, Zhang H, Wang J, Zhong Y, Lai Z, Xiang J, Shan PF, Zheng JS, Wang H, Zhu Y, Guo T
Cell (Dec 2025)

Population aging is accelerating, yet the multi-organ aging process and the geroprotective effects of dietary protein restriction (PR) remain poorly understood. Here, we conducted comprehensive proteomic analyses on 41 mouse tissues during male mouse aging and PR. Our findings identified tissue-specific aging hallmarks, including widespread changes in immunoglobulins and serine protease inhibitors across multiple tissues. PR mitigated age-related tissue-specific protein expression, epigenomic states, and protein phosphorylation patterns, and it significantly improved adipose tissue functions. These findings were supported by independent reduced representation bisulfite sequencing (RRBS), phosphoproteomics, and pathological analyses. Furthermore, analysis of plasma samples from mice and humans confirmed the cardiovascular benefits of PR. We identified sexual and temporal variations in the impact of PR, with middle age being the optimal intervention period. Overall, our study depicts the multi-organ aging process and provides valuable insights into the geroprotective potential of PR.]]> Wed, 31 Dec 1969 19:00:00 EST