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        <title>Frontiers in Genetics | RNA section | New and Recent Articles</title>
        <link>https://www.frontiersin.org/journals/genetics/sections/rna</link>
        <description>RSS Feed for RNA section in the Frontiers in Genetics journal | New and Recent Articles</description>
        <language>en-us</language>
        <generator>Frontiers Feed Generator,version:1</generator>
        <pubDate>2026-05-09T18:51:33.840+00:00</pubDate>
        <ttl>60</ttl>
        <item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fgene.2026.1773468</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fgene.2026.1773468</link>
        <title><![CDATA[Diverse roles of YTHDC1 in chromatin and blood cancers]]></title>
        <pubdate>2026-05-08T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Baptiste Pernon</author><author>Yacine Benchikh</author><author>Cyril Fournier</author><author>Maxime Delforge</author><author>Baptiste Dumétier</author><author>Laurent Delva</author><author>Amandine Durand</author><author>Cédric Rossi</author><author>Laurent Martin</author><author>Fabien Guidez</author><author>André Verdel</author><author>Romain Aucagne</author><author>Mary B. Callanan</author>
        <description><![CDATA[Epitranscriptomics, the study of RNA modifications, together with their functional characterization, is emerging as an important area of investigation in RNA biology. Of the over 170 RNA modifications that have been identified on mRNA and non-coding RNAs, N6-methyladenosine (m6A) modification to mRNA is recognized as a key regulator of gene expression, splicing and protein translation. Functional readout of m6A is mediated by m6A readers mostly in the cytoplasm except for the nuclear-localized YTHDC1. m6A-YTHDC1 function has recently been extended to include short and long-range fine-tuning of genome activity via chromatin-associated mechanisms. This review summarizes YTHDC1-m6A nuclear functions in normal and cancer cells with special focus on its chromatin-associated roles and the ability of YTHDC1 to assemble into higher order nuclear structures called condensates. These processes are disturbed in cancer.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fgene.2026.1825784</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fgene.2026.1825784</link>
        <title><![CDATA[RUNX1-mediated repression of miR-24 promotes hepatic stellate cell activation and liver fibrosis by targeting the ALK4/Smad3 signaling pathway]]></title>
        <pubdate>2026-04-30T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Zhijing Wang</author><author>Meiyi Song</author><author>Yingying Zhao</author><author>Jing Li</author><author>Lu Xia</author><author>Fei Wang</author><author>Changqing Yang</author>
        <description><![CDATA[BackgroundEpigenetic mechanisms, including microRNAs (miRNAs), are increasingly recognized as crucial regulators of organ fibrosis. In this study, we investigated the role of miR-24 in hepatic stellate cell (HSC) activation and liver fibrosis.MethodsmiR-24 expression was analyzed in carbon tetrachloride (CCl4)-induced liver fibrosis and activated HSCs using quantitative real-time PCR (qRT-PCR). Gain- and loss-of-function experiments of miR-24 were performed in vitro. Western blotting, qRT-PCR, 5-ethynyl-2′-deoxyuridine (EdU) staining, flow cytometry, luciferase reporter assays, bioinformatics analysis, and chromatin immunoprecipitation PCR (ChIP-PCR) were performed to examine the molecular mechanisms of miR-24. Serum miR-24 levels were measured in patients with liver cirrhosis and further analyzed by subgroup.ResultsWe observed significant downregulation of miR-24 in CCl4-induced liver fibrosis and activated HSCs. Functional assays showed that miR-24 overexpression markedly inhibited HSC activation and migration, whereas miR-24 inhibition had the opposite effects. Mechanistically, ALK4 was identified as a direct target of miR-24: miR-24 bound the 3′UTR of ALK4 mRNA, thereby suppressing Smad3 phosphorylation and downstream fibrosis-associated signaling pathways. Furthermore, the transcription factor RUNX1 was induced during HSC activation, and it transcriptionally repressed miR-24 expression. Clinically, serum miR-24 levels were significantly lower in patients with liver cirrhosis than in healthy controls and were negatively correlated with Child–Pugh grade.ConclusionOur findings suggest that the RUNX1/miR-24/ALK4 axis plays a crucial role in HSC activation and migration. miR-24 may serve as a biomarker for liver fibrosis screening, representing a potential therapeutic target for anti-fibrotic intervention.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fgene.2026.1781941</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fgene.2026.1781941</link>
        <title><![CDATA[Single cell and single nucleus RNA sequencing in liver tissues: applications and prospects in model and non-model organisms]]></title>
        <pubdate>2026-04-28T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Xue Feng</author><author>Yu Feng</author><author>Sayed Haidar Abbas Raza</author><author>Yun Ma</author><author>Hongyu Deng</author>
        <description><![CDATA[The liver serves as a central metabolic hub, essential for homeostasis, detoxification, and immunity. Recent advances in single-cell and single-nucleus RNA sequencing (scRNA-seq and snRNA-seq) have fundamentally transformed our capacity to resolve the cellular architecture and functional states of this complex organ. This review comprehensively examines the pivotal applications and expanding potential of these high-resolution transcriptomic technologies in hepatic research, encompassing both established model organisms and emerging non-model species. In human and classical models such as mice and zebrafish, scRNA-seq and snRNA-seq have been critical for delineating developmental trajectories, deciphering the molecular logic of metabolic zonation, and uncovering the precise cellular dynamics and intercellular communication networks that drive diseases like non-alcoholic fatty liver disease (NAFLD), fibrosis, and hepatocellular carcinoma. Beyond these systems, pioneering work in species such as cattle, pigs, tree shrews, and reptiles is now providing unique insights into evolutionary adaptations, specialized physiologies, and comparative disease mechanisms. By synthesizing findings across this broad biological spectrum, we illustrate how single-cell transcriptomics is refining the core principles of liver biology while simultaneously revealing species-specific divergences. Looking ahead, the continued maturation and application of these technologies are poised to yield deeper comparative pathophysiological understanding and accelerate the development of targeted diagnostic and therapeutic strategies for liver diseases in both human and veterinary contexts.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fgene.2026.1770769</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fgene.2026.1770769</link>
        <title><![CDATA[Nanopore-m6A-finder, a novel m6A site caller for Nanopore DRS data]]></title>
        <pubdate>2026-04-22T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Yuening Yang</author><author>Liqun Yu</author><author>Li Mo</author><author>Changhai Qi</author><author>Wei Song</author><author>Hua Jin</author>
        <description><![CDATA[IntroductionN6-methyladenosine (m6A) is a pivotal RNA modification involved in diverse biological and pathological processes. Compared to the m6A detection methods based on second-generation sequencing, Nanopore direct RNA sequencing (DRS) offers the unique advantage of capturing native modifications.MethodsHere, we present Nanopore-m6A-Finder (NP-mFinder), a reference-free m6A prediction computational framework that employs the XGBoost model in the mRNA exonic region and a hard-voting ensemble of XGBoost and random forest models in the poly(A) region.Results and discussionNP-mFinder can determine m6A sites as well as estimate their methylation levels from Guppy basecalled DRS data. After training with DRS data of in vitro-transcribed RNA, NP-mFinder achieved high performance on held-out test datasets (area under the curve (AUC) ≈0.90; accuracy, precision, recall, and F1-score >0.80). Comparing with canonical m6A detection methods, it recovered 20% of meRIP-seq-defined m6A sites in yeast, and 27% of our HEK293 site prediction overlapped with miCLIP calls. Although single-base overlap with existing DRS-based tools of EpiNano and mAFiA was limited, 73% of our identified m6A-containing genes were validated by at least one of them. Benchmarking our method with GLORI v2.0 revealed concordance of 28% at a site level and 85% at a gene level, as well as a mild correlation on m6A level estimations. Notably, NP-mFinder achieved 93% precision in detecting m6A within the “AAAAA” sequence context in the mRNA exonic region of HEK293T DRS data when compared to high-confidence m6A site annotation in GLORI v2.0, demonstrating the good performance of our method in the region possessing a stretch of continuous A-sequences. Moreover, our method predicted that m6A might exist in the human HEK293 poly(A) region, suggesting a possibly conserved phenomenon of a modified poly(A) tail beyond the previously reported T. brucei variant surface glycoprotein (VSG) transcripts. Together, these results established NP-mFinder as a robust and versatile tool for transcriptome-wide m6A profiling with DRS data at single-read resolution.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fgene.2026.1813517</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fgene.2026.1813517</link>
        <title><![CDATA[Brave new RNA world(s): from prebiotic chemistry to gene regulation and RNA technology]]></title>
        <pubdate>2026-04-15T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Alexis A. Flores-García</author><author>Aura Hernandez-Rodriguez</author><author>E. Isabel López-Brito</author><author>Dafne F. Nava-Domínguez</author><author>Sebastian P. Pasapera</author><author>R. Franchesca Pazos-Murillo</author><author>Tonatzin Pineda-Diaz</author><author>Alberto Vázquez-Salazar</author>
        <description><![CDATA[RNA has long provided a plausible route by which heredity and catalysis could become linked in early evolution, and the same chemical versatility helps explain why RNA remains central to origin-of-life research, modern cell biology, and biotechnology. This review adopts a plural framing of RNA worlds to connect three regimes: a primordial RNA world constrained by geochemistry, a contemporary RNA world in which RNAs contribute to catalysis and regulation in cells, and an applied RNA world in which RNA is engineered as a programmable tool. Across these regimes, a common logic emerges from the mapping of sequence to structure to function under explicit constraints. In early evolution, cycling, interfaces, and confinement can generate heterogeneous oligomer pools and bias their persistence, whereas the transition toward Darwinian dynamics depends on copying fidelity, strand dynamics, and compartment coupled population structure. In cells and applications, noncoding RNA networks, RNA modifications, and RNA-guided targeting implement specificity in chemically complex environments, while laboratory selection and design must also confront constraints imposed by stability, delivery, and immune sensing. Across contexts, fitness landscapes and tradeoffs between peak performance and robustness provide experimental benchmarks and practical design principles for RNA function.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fgene.2026.1787421</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fgene.2026.1787421</link>
        <title><![CDATA[Tumor microenvironment-induced epigenetic reprogramming of Tregs and its impact on immunotherapy]]></title>
        <pubdate>2026-03-27T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Wenhao Li</author><author>Jiyu Tong</author>
        <description><![CDATA[The tumor microenvironment (TME) represents a complex system comprising various cells and extracellular matrix components that play a crucial role in tumor initiation and progression. While recent therapeutic strategies for predominantly focus on targeting tumor cells, their impact on other cellular components in the TME, such as regulatory T (Treg) cells, remains insufficiently understood. The cellular components of the TME include tumor cells, immune cells, tumor-associated stromal cells, and myeloid-derived suppressor cells. Notably, the role of Treg cells in tumor therapy has emerged as a significant research area of focus in recent years. Regulatory CD4+ T cells, characterized by the expression of the transcription factor Forkhead Box P3 (FOXP3) and the surface marker CD25, are pivotal in mediating immune suppression and maintaining immune tolerance and homeostasis. Current tumor treatments mainly rely on radiation and chemotherapy. Although innovative therapies such as immune checkpoint inhibitors (ICIs) and chimeric antigen receptor T-cell (CAR-T) therapies have demonstrated promising outcomes, their efficacy is limited, benefiting only a small subset of patients. Epigenetic inhibitors are increasingly recognized as pivotal in cancer treatment; however, prior research has predominantly concentrated on their effects on the tumor itself, while overlooking the potential influence of these compounds on regulatory T cells (Tregs) within the tumor microenvironment (TME). The therapeutic viability of modulating Tregs within the TME remains uncertain. The intricate microenvironment of the TME significantly influences the distinct epigenetic landscape of tumor-infiltrating Treg cells, including modifications in DNA methylation, histone modifications, and chromatin remodeling. A comprehensive understanding of these epigenetic modifications and the underlying factors driving them could unveil novel strategies for cancer therapy. This approach would enhance the understanding of the critical role of Tregs in tumor therapy and facilitate the development of more effective targeted therapies by addressing the unique epigenetic characteristics of tumor-infiltrating Tregs.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fgene.2026.1814124</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fgene.2026.1814124</link>
        <title><![CDATA[Correction: Association of mir-196a-2 rs11614913 and mir-149 rs2292832 polymorphisms with risk of cancer: an updated meta-analysis]]></title>
        <pubdate>2026-03-25T00:00:00Z</pubdate>
        <category>Correction</category>
        <author>Jalal Choupani</author><author>Ziba Nariman-Saleh-Fam</author><author>Zahra Saadatian</author><author>Elaheh Ouladsahebmadarek</author><author>Andrea Masotti</author><author>Milad Bastami</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fgene.2026.1806282</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fgene.2026.1806282</link>
        <title><![CDATA[THGC_MDA: a method for predicting the associations between m1A modification and diseases based on ternary heterogeneous network and graph convolutional neural network]]></title>
        <pubdate>2026-03-20T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Hongyan Gao</author><author>Xue Zhou</author><author>Lei Bai</author><author>Haifeng Yang</author><author>Fei Liu</author>
        <description><![CDATA[m1A modification, as a pivotal RNA epigenetic modification, plays a central regulatory role in the pathogenesis and progression of complex human diseases, including cancer. Exploring the potential associations between m1As and diseases are an important approach to revealing the molecular mechanism of disease onset. However, traditional biological experiments have the limitations of time-consuming and labor-intensive, resulting in an extremely scarce amount of verified m1A-disease association data. Meanwhile, the existing computational prediction methods are mostly limited to specific application scenarios and rely solely on the direct correlation data between m1As and diseases. They do not fully integrate multi-dimensional biological information and thus are unable to achieve efficient and accurate association predictions. In view of this, this study proposes a method for predicting the association between m1A modification and diseases based on a ternary heterogeneous network and GCN. By introducing circRNA as an intermediate connection node, a ternary association network of m1A-circRNA-disease is constructed, which effectively enriches the dimension of feature information for both m1A and diseases. Meanwhile, leveraging the feature learning capability of Graph Convolutional Network, the extraction and representation of their features are realized. The experimental results demonstrate that the proposed approaches significantly outperforms existing mainstream methods in predictive performance, substantially enhancing the accuracy and reliability of m1A-disease association prediction. Furthermore, case validation has further confirmed that the predicted candidate m1A sites participate in regulating disease-related gene expression networks by modulating core processes such as RNA localization, stability, and translation efficiency, thereby providing novel insights into the investigation of disease pathogenesis.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fgene.2026.1760431</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fgene.2026.1760431</link>
        <title><![CDATA[miR-18a-5p promotes phenotypic transformation of airway smooth muscle cells by targeting SPRY1 to activate the RAS-MAPK pathway]]></title>
        <pubdate>2026-03-19T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Lijuan Hu</author><author>Lei Li</author>
        <description><![CDATA[ObjectiveThis study investigates the role of miR-18a-5p in the phenotypic transformation of airway smooth muscle cells (ASMCs) and its underlying mechanism in asthma-related airway remodeling.MethodsExpression of miR-18a-5p in sputum from asthma patients was assessed by RT-qPCR. An in vitro model was established by stimulating ASMCs with TGF-β1. The responsiveness of miR-18a-5p expression to asthma-related mitogenic stimulation was also evaluated. ASMC proliferation and migration were evaluated following miR-18a-5p overexpression or inhibition using CCK-8 and Transwell assays. Western blot was used to detect migration-associated proteins, phenotypic markers and activation of the RAS-MAPK pathway. The regulatory relationship between miR-18a-5p and SPRY1 was validated by dual-luciferase assay, and SPRY1 knockdown was performed to explore its functional role.ResultsmiR-18a-5p was significantly upregulated in asthma patients. Overexpression of miR-18a-5p promoted ASMC proliferation and migration, accompanied by upregulation of migration-related proteins (Integrin β1,p-FAK/FAK,p-Paxillin/Paxillin,MMP9), increased synthetic phenotype markers (α-SMA, OPN, Collagen I/III), and reduced contractile marker (Calponin). It also activated the RAS-MAPK pathway. SPRY1 was confirmed as a direct target of miR-18a-5p. Knockdown of SPRY1 reversed the effects of miR-18a-5p inhibition, confirming its role in mediating ASMC phenotypic changes.ConclusionmiR-18a-5p promotes ASMC phenotypic switching and airway remodeling in asthma by targeting SPRY1 and activating the RAS-MAPK signaling pathway. These findings suggest miR-18a-5p as a potential therapeutic target for asthma.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fgene.2026.1788918</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fgene.2026.1788918</link>
        <title><![CDATA[Molecular mediators of motion: RNA–RBP networks in exercise-induced osteoarthritis protection]]></title>
        <pubdate>2026-03-12T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Yupeng Yang</author><author>Xue Wang</author><author>Xuchang Zhou</author><author>Ying Li</author><author>Yinghao Shen</author><author>Zhujun Mao</author><author>Junjie Liu</author><author>Mi Zheng</author>
        <description><![CDATA[Osteoarthritis (OA) is a relatively common chronic degenerative disease of joints that was originally considered an imbalance between mechanical loads and tissue repair. Emerging evidence indicates that exercise confers protection not merely through mechanical loading, but also by acting as a systemic regulator of RNA metabolism. This modulation mainly happens by regulating RNA–RNA-binding protein interaction networks that can regulate joint homeostasis and delay the OA process. This article is a review of current understanding of how physical activity alters networks of RNA–RNA-binding proteins (RBPs) in different joint-related tissues, such as cartilage, synovium, skeletal muscle, and systemic circulation, and changes the metabolic and inflammatory pathways necessary for joint health. The article will examine molecular mechanisms by which exercise induces RNA metabolism reprogramming and protection from OA. It also studies the promising prospects of RNA–RBP networks in early detection of OA and targeting innovative treatment strategies. By combining what we know about RNA–RBP interaction with exercise physiology, this overview could clear the way to personalized exercise interventions and novel RNA-targeted therapies for OA.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fgene.2026.1775005</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fgene.2026.1775005</link>
        <title><![CDATA[Exercise stress and tissue remodeling: advances in exosome-mediated RNA–RBP networks in musculoskeletal injury repair and functional recovery]]></title>
        <pubdate>2026-03-11T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Junjie Liu</author><author>Heming Chen</author><author>Yupeng Yang</author><author>Zheheng Jia</author><author>Ying Li</author><author>Xintong Zhong</author><author>Huimei Jiang</author><author>Zhujun Mao</author><author>Mi Zheng</author>
        <description><![CDATA[Exercise is a double-edged sword. It can either cause adaptive remodeling of musculoskeletal tissues or lead to acute or chronic injury. Exosomes that are boosted with circular RNAs (circRNAs), long non-coding RNAs (lncRNAs), and RNA-binding proteins (RBPs) have been a focus in recent years as important contributors to the process of repair after exposure to stress during exercise. This narrative review is a summarization of the impacts of different types and intensities of exercise modalities on musculoskeletal patterns of RNA expression and exosome secretion. It also describes the role of exosomes that initiate RNA–RBP networks that coordinate regenerative and inflammatory reactions in recipient cells. The article notes the promise of these networks as diagnostic biomarkers and therapeutic targets and also suggests new clinical uses, such as engineered exosome-based interventions. This review will build a holistic but theoretically sound framework to inform future direct-to-patient research in exercise medicine by taking into account multi-omics data and its functional validation. The purpose of this article is to present better diagnostic and rehabilitative approaches to musculoskeletal injuries, leading to suitable functional recovery outcomes.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fgene.2026.1753495</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fgene.2026.1753495</link>
        <title><![CDATA[Aberrant expression of the MID1 protein in neurons of Huntington’s disease brain]]></title>
        <pubdate>2026-03-11T00:00:00Z</pubdate>
        <category>Brief Research Report</category>
        <author>Adriana Geraci</author><author>Annika Reisbitzer</author><author>Janina Gerhard</author><author>Sybille Krauß</author>
        <description><![CDATA[Huntington’s disease (HD) is caused by a CAG repeat expansion mutation in the Huntingtin (HTT) gene that transcribes into mRNA and translates into a polyglutamine tract. The mutant HTT gene products drive pathological changes that result in neurodegeneration. The mutant CAG repeat RNA contributes to cellular dysfunction by aberrantly recruiting RNA-binding proteins. For example, the mutant HTT transcript associates with a protein complex containing the MID1 protein. This aberrant recruitment of the MID1 protein complex results in an increased translation of mutant HTT. MID1 expression is abnormally high in both the brains of HD mouse models and HD patients. However, the cell type in which MID1 is overexpressed in HD brains remains obscure. Here, we investigated the MID1 expression in different brain cell types of an HD mouse model. Therefore, we separated neurons, astrocytes and microglia via magnetic sorting and show that MID1 is overexpressed in neurons of an HD mouse model. Moreover, we stained MID1 in brain sections of HD mice via immunohistochemistry and observed MID1 overexpressing cells in cortex. This finding shows that MID1 is highly expressed in neurons–the most vulnerable cell type in HD–underlining its important role in the neurodegenerative process. This supports the concept of blocking the interaction between MID1 and mutant HTT mRNA to counteract mutant HTT translation as a promising therapeutic approach.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fgene.2026.1749292</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fgene.2026.1749292</link>
        <title><![CDATA[Correction: A comprehensive analysis of the prognostic characteristics of microRNAs in breast cancer]]></title>
        <pubdate>2026-03-11T00:00:00Z</pubdate>
        <category>Correction</category>
        <author>Lingying Wang</author><author>Gui Wang</author><author>Jiahong Song</author><author>Di Yao</author><author>Yong Wang</author><author>Tianyou Chen</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fgene.2026.1718719</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fgene.2026.1718719</link>
        <title><![CDATA[Research advancements on the role of CircRNAs in cartilage injury within osteoarthritis]]></title>
        <pubdate>2026-03-06T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Chengri Liu</author><author>Yanqun Liu</author><author>Baojian Zhang</author><author>Qingyu Xu</author>
        <description><![CDATA[The main causes of articular cartilage injury (ACI) encompass inflammation, trauma, chronic strain, degeneration, and so forth. ACI is one of the main pathological features of degenerative joint diseases such as osteoarthritis (OA), which significantly affects patients' normal work and life. Due to the absence of nerves, blood vessels, and lymphatic tissue in the cartilage, it is challenging for it to repair itself after injury.​ Non-coding RNAs, as crucial regulators of gene expression, have been increasingly implicated in the pathophysiology of various diseases. Among them, circular RNAs(circRNAs), as a new type of endogenous special non-coding RNAs, have been extensively discovered in eukaryotic cells. Owing to their unique closed-loop structure and potentially stable expression characteristics, circRNAs have demonstrated significant regulatory roles in the occurrence and development of various diseases. circRNAs are differentially expressed in OA chondrocytes and normal chondrocytes, and are involved in the inflammatory response, proliferation, apoptosis, and other processes of chondrocytes and the extracellular matrix (ECM). This article aims to review the recent research progress of circRNAs in ACI and explore their potential role in the pathogenesis of OA.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fgene.2026.1776616</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fgene.2026.1776616</link>
        <title><![CDATA[m6AHD: a new framework for identifying abnormal N6-methyladenosine (m6A) in heart diseases based on sequencing features]]></title>
        <pubdate>2026-02-25T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Jiajie Lu</author><author>Yanan Li</author><author>Yuxiang Hong</author><author>Dongshan Liao</author><author>Guanhua Fang</author>
        <description><![CDATA[IntroductionCardiovascular disease (CVD) is a major threat to health, with high incidence rates and a trend toward younger age groups. RNA modifications are an important component of epigenetics, widely present and indispensable in cells. Increasing evidence suggests that RNA modifications are key regulatory factors involved in cardiac physiological and pathological changes. Understanding the role of RNA modifications in heart-related diseases can help us to identify new drug targets.MethodsTo systematically investigate the role of m6A modification in different cardiac diseases, we integrated m6A epitranscriptome profiles from five cardiac pathological conditions (three drug-induced cardiac toxicity models—Evodiamine, Matrine, and TKI, hypertrophy, and heart calcification) and their control groups to construct the first predictive model for abnormal m6A modification in cardiac diseases. We constructed separate models for upregulated and downregulated modifications under different pathological conditions, performed feature selection and parameter optimization, and validated the performance of our models using an independent test set.Resultsm6AHD demonstrated excellent performance on the independent test set, with AUROC scores ranging from 0.728 to 0.880 across various pathological conditions. Cross-validation across different conditions and model interpretability demonstrated that m6A modifications exhibit similar patterns under different pathological conditions and are potentially regulated by similar factors, providing new clues for identifying targets in cardiovascular diseases at the epitranscriptome level. Furthermore, we validated our findings using a zebrafish model of Evodiamine-induced cardiotoxicity. The experimental results revealed significant morphological defects and a broad downregulation of m6A methyltransferase complex components, confirming the involvement of aberrant m6A machinery in the pathology of cardiotoxicity.Discussionm6AHD is the first dedicated framework for predicting multi-condition cardiac m6A dysregulation. Our findings underscore the critical role of m6A homeostasis in cardiomyocyte function and demonstrate that aberrant methylation patterns can serve as reliable indicators of cardiac pathology. This framework provides a robust computational tool for identifying potential therapeutic targets at the epitranscriptome level for cardiovascular diseases.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fgene.2026.1781271</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fgene.2026.1781271</link>
        <title><![CDATA[Emerging role of epigenetic mechanisms in glaucoma and their translational potential]]></title>
        <pubdate>2026-02-23T00:00:00Z</pubdate>
        <category>Mini Review</category>
        <author>Altaf A. Kondkar</author><author>Tahira Sultan</author><author>Taif A. Azad</author><author>Saleh A. Al-Obeidan</author>
        <description><![CDATA[Glaucoma, a leading cause of irreversible blindness, is a complex polygenic disease where significant clinical and genetic heterogeneity do not explain all glaucoma cases, highlighting the need for a deeper understanding of molecular mechanisms like epigenetics. This review examines the emerging role of key epigenetic mechanisms, specifically DNA methylation, histone modifications, and non-coding RNAs in glaucoma pathogenesis and their potential as biomarkers and therapeutic targets. We discuss how aberrant DNA methylation (e.g., GDF7 hypomethylation/CDKN2B hypermethylation) promotes trabecular meshwork fibrosis and increases optic nerve vulnerability, contributing to disease development and/or progression. The METTL23 histone methylation linked to retinal ganglion cell death at normal eye pressure, and disease-specific microRNA profiles further support the role of epigenetic involvement in glaucoma. The proof-of-concept studies of GDF7 neutralization in primate models and the OSK-factor reprogramming in aged and glaucoma mice models, show that epigenetic changes are reversible and can restore visual functions. DNA methylation-based epigenetic clocks identify glaucoma as an accelerated molecular aging process. Although promising, the current evidences are largely preclinical and long-term human data are still lacking. Nonetheless, the inherent reversible nature of epigenetics offers significant translational potential. Methylation, epigenetic clocks, and circulating microRNA profiles could enable early, non-invasive biomarkers for diagnosis and prognosis. Future efforts are needed to validate biomarkers in large cohorts and develop targeted epigenetic therapies. In conclusion, epigenetics is redefining our current understanding of glaucoma from a pressure-based disease to a modifiable link between genes and environment paving the way for personalized care for vision preservation beyond pressure-lowering treatments.]]></description>
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        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fgene.2026.1775625</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fgene.2026.1775625</link>
        <title><![CDATA[RNA-triggered innate immunity: friend and foe]]></title>
        <pubdate>2026-02-23T00:00:00Z</pubdate>
        <category>Mini Review</category>
        <author>Maike Henschel</author><author>Maria R. Conte</author><author>Rocio T. Martinez-Nunez</author>
        <description><![CDATA[Endogenous, or ‘self’, vs. microbial, or ‘non-self’, RNA sensing can tip the scales between immune pathology and effective immunity. Cells are equipped to sense RNA, fundamental to trigger an innate immune response to clear viral infection that should not generate a harmful immune response against endogenous RNA. Multiple chemical modifications in RNA fine-tune its cellular sensing and are exploited by pathogens to evade immunity. Likewise, perturbations triggering self RNA sensing cause immune pathologies. This underscores the clinical need for a better understanding of self RNA recognition. Here, we address nucleic acid sensing in the innate immune response from an RNA-centric view. We discuss how self RNA is shielded from sensing by chemical modifications and subcellular compartmentalization, possible mechanisms and consequences of self-RNA sensing, and how this knowledge has been harnessed to revolutionize vaccine development.]]></description>
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        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fgene.2026.1769972</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fgene.2026.1769972</link>
        <title><![CDATA[The role of miRNAs in the development of brain metastases originating from lung adenocarcinoma]]></title>
        <pubdate>2026-02-20T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Bernadett Torner</author><author>Álmos Klekner</author><author>István Balogh</author><author>András Penyige</author><author>Dóra Géczi</author><author>Tekla Gáspár</author><author>Gréta Geszti</author><author>Zsuzsanna Birkó</author>
        <description><![CDATA[IntroductionBrain metastases (BMs) represent most malignant lesions of the central nervous system. Lung cancer—particularly lung adenocarcinoma (LUAD, ∼25%)—is the most common source of BMs. MicroRNAs (miRNAs) play a crucial role in regulating gene expression, thereby contributing to tumor progression and metastatic spread. Identifying these regulatory molecules may enable a deeper understanding of the mechanisms driving LUAD brain metastasis (LUAD-BM) development and reveal therapeutic targets to prevent or limit disease progression.MethodsNext-generation RNA sequencing (RNA-seq) was performed on six LUAD-BM and six non-tumorous human brain tissue samples to assess miRNA expression profiles. Additionally, RNA-seq data from 20 primary LUAD and 15 normal lung tissue samples were obtained from The Cancer Genome Atlas (TCGA) database. MiRNAs showing the most pronounced alterations in LUAD-BM samples were selected for validation by real time quantitative polymerase chain reaction (RT-qPCR).ResultsAnalysis of RNA-seq data identified 229 differentially expressed (DE) miRNAs between LUAD-BM and control samples. Functional annotation analysis indicated that these DE miRNAs are key regulators of tumorigenesis and metastasis. Using the Mann–Whitney U test, ten miRNAs were confirmed to differ significantly between LUAD-BM and normal brain tissue. Receiver operating characteristic (ROC) curve analysis demonstrated their diagnostic potential. Among the ten validated miRNAs, miR-200c-3p, miR-146b-5p, and miR-3934-5p showed distinct expression patterns between primary LUAD and LUAD-BM, while miR-10a-5p, miR-210-3p, and miR-130b-3p exhibited stepwise dysregulation along the normal lung–LUAD–LUAD-BM axis, suggesting their involvement in metastatic progression.ConclusionWe identified ten miRNAs that showed preliminary ability to differentiate LUAD-BM from normal brain tissue. These findings indicate possible diagnostic and therapeutic implications. Among these, six miRNAs showed significant expression changes along the normal control–primary LUAD–LUAD-BM axis, highlighting their potential as biomarkers and therapeutic targets in BM development.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fgene.2026.1772541</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fgene.2026.1772541</link>
        <title><![CDATA[Regulatory roles of the circRNA–RBP axis in exercise-induced skeletal muscle remodeling: mechanistic controversies and translational illusions]]></title>
        <pubdate>2026-02-20T00:00:00Z</pubdate>
        <category>Mini Review</category>
        <author>Junjie Liu</author><author>Yupeng Yang</author><author>Heming Chen</author><author>Mingming Liu</author><author>Zhujun Mao</author><author>Mi Zheng</author>
        <description><![CDATA[Metabolic health and physical performance rely upon skeletal muscle adaptation that is a result of exercise. Recent advancements in high-throughput sequencing and functional genomics have successfully identified a vast landscape of exercise-responsive circRNAs, providing critical insights into the molecular complexity of muscle adaptation. While these studies have established a foundational framework for understanding the circRNA–RBP axis, there are serious issues related to current research. There are serious issues related to current research: an insufficient level of endogenous circRNA to produce substantial ceRNA effects, unconfirmed circRNA scaffolding due to overactivity of RBPs, poor conservation of so-called exercise-related circRNAs evolutionarily, and the over-interpretation of specific effects. The article focuses on basic concerns of the ceRNA model quantitative limitations, and specificity debate of the scaffolding model, current model and technical gaps, etc. and suggests an experimental framework transitioning from “narrative models” to “physiologically credible mechanisms,” offering references for future rigorous research and elucidating the authentic role of the circRNA–RBP axis.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fgene.2026.1566012</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fgene.2026.1566012</link>
        <title><![CDATA[Identification of key biomarkers of telomere-related genes in diabetic nephropathy via bioinformatic analysis]]></title>
        <pubdate>2026-02-04T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Dan Yu</author><author>Zhipeng Feng</author><author>Huan Yao</author><author>Ke An</author>
        <description><![CDATA[BackgroundDiabetic nephropathy (DN) is a major cause of end-stage renal disease. Understanding the molecular mechanisms underlying DN is crucial for developing new therapeutic targets and diagnostic biomarkers.MethodsWe utilized microarray data from the GEO database to identify differentially expressed genes related to DN. Machine learning algorithms, including LASSO regression and SVM-RFE, were employed to screen and validate telomere-related genes. We also predicted the transcription factors of the significant genes. Subsequently, correlation analysis and Receiver Operating Characteristic diagnostics were performed on the key genes, along with validation using external datasets. Additionally, GSEA enrichment analysis and immune infiltration analysis were conducted. Furthermore, we analyzed the expression of significant genes in cell subgroups using single-cell sequencing technology. Finally, key genes were validated in DN kidney biopsy tissues and normal kidney biopsy tissues.ResultsThrough differential analysis and machine learning screening, we identified a total of 14 differentially expressed genes related to telomeres, among which TRIM22, ELOVL4, NLGN4X, and FOSB were highlighted as key genes. We also predicted seven related transcription factors (BCLAF1, HNRNPL, TAF15, STAT1, SRSF9, SAFB2, PTEN). The key gene TRIM22 showed a high correlation with NLGN4X, ELOVL4, and NLGN4X. ROC diagnostics demonstrated sufficient diagnostic accuracy in both the test and validation sets. GSEA enrichment analysis and immune infiltration analysis revealed significant differences among immune cells, such as PC cells, and preliminary expression validation was conducted using single-cell analysis (for example, TRIM22 exhibited high expression levels in EDC, PEC, MES, and IMC). Finally, we performed RT-PCR between DN samples and control samples, finding that the expression levels of key genes in both groups were consistent with the trends predicted by bioinformatics, indicating that these genes may serve as potential diagnostic biomarkers and therapeutic targets.ConclusionThis study provides a comprehensive analysis of telomere-related DEGs in DN, enhancing our understanding of DN pathogenesis. The identified key genes offer potential for new diagnostic and therapeutic strategies, warranting further investigation into their biological roles in DN.]]></description>
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