Non-Coding RNA最新文献

{"title":"The Stiff Side of Cancer: How Matrix Mechanics Rewrites Non-Coding RNA Expression Programs.","authors":"Alma D Campos-Parra, Jonathan Puente-Rivera, César López-Camarillo, Stephanie I Nuñez-Olvera, Nereyda Hernández Nava, Gabriela Alvarado Macias, Macrina Beatriz Silva-Cázares","doi":"10.3390/ncrna12010007","DOIUrl":"10.3390/ncrna12010007","url":null,"abstract":"<p><p>Extracellular matrix (ECM) stiffening is a defining biophysical feature of solid tumors that reshape gene regulation through mechanotransduction. Increased collagen crosslinking and stromal remodeling enhance integrin engagement, focal-adhesion signaling and force transmission to the nucleus, where key hubs such as lysyl oxidase (LOX), focal adhesion kinase (FAK) and the Hippo co-activators YAP1 and TAZ (WWTR1) promote proliferation, invasion, stemness and therapy resistance. Here, we synthesize evidence that quantitative changes in matrix stiffness remodel the miRNome and lncRNome in both tumor and stromal compartments, including extracellular vesicle cargo that reprograms metastatic niches. To address heterogeneity in experimental support, we classify mechanosensitive ncRNAs into studies directly validated by stiffness manipulation (e.g., tunable hydrogels/AFM) versus indirect associations based on mechanosensitive signaling, and we summarize physiological versus pathophysiological stiffness ranges across tissues discussed. We further review competing endogenous RNA (ceRNA) networks converging on mechanotransduction nodes and ECM remodeling enzymes, and discuss translational opportunities and challenges, including targeting mechanosensitive ncRNAs, combining ncRNA modulation with anti-stiffening strategies, delivery barriers in dense tumors, and the potential of circulating/exosomal ncRNAs as biomarkers. Overall, integrating ECM mechanics with ncRNA regulatory circuits provides a framework to identify feed-forward loops sustaining aggressive phenotypes in rigid microenvironments and highlights priorities for validation in physiologically relevant models.</p>","PeriodicalId":19271,"journal":{"name":"Non-Coding RNA","volume":"12 1","pages":""},"PeriodicalIF":4.2,"publicationDate":"2026-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12943065/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147290600","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Computational Analysis of Telomerase RNA Evolution in <i>Caenorhabditis</i> Species.","authors":"Christopher Klapproth, Franziska Reinhardt, Peter F Stadler, Sven Findeiß","doi":"10.3390/ncrna12010006","DOIUrl":"10.3390/ncrna12010006","url":null,"abstract":"<p><p><b>Background/Objectives:</b> The telomerase RNA (TR) is an indispensable part of the telomerase protein complex responsible for telomere elongation in most eukaryotic species. Although the telomere terminal repeat sequence (TTAGGC)_n in <i>Caenorhabditis elegans</i> has been known for years, a telomerase RNA gene was not identified in the entire phylum of Nematoda until recently. <b>Methods:</b> In this exploratory study, we employ a combination of different approaches to identify likely telomerase RNA candidates among putative non-coding transcripts. <b>Results:</b> A detailed analysis of our prime candidate shows compelling evidence that it encodes the missing RNA element of the telomerase complex, which is notably located in an intron of the coding gene <i>nmy-2</i>. Using <i>nmy-2</i> homologs in other nematodes as anchors, we annotate the conserved TR gene in 21 <i>Caenorhabditis</i> species. We furthermore show that the intronic localization of the TR gene is conserved in two distinct branching groups of the <i>Caenorhabditis</i> phylogeny and demonstrate that this property likely emerged from a single point of origin. <b>Conclusions:</b> While the intronic TR represents a very interesting evolutionary adaption that seems to have been successful in the Elegans and Japonica groups, the question regarding the macroscopic nematode TR evolution remains.</p>","PeriodicalId":19271,"journal":{"name":"Non-Coding RNA","volume":"12 1","pages":""},"PeriodicalIF":4.2,"publicationDate":"2026-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12921731/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146259006","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Extracellular Small RNAs in Human Milk: Molecular Profiles, Stability and Fragment-Specific Responses in Cell-Based Assays.","authors":"Clara Claus, Carla Borini Etichetti, Bruno Costa, Julieta B Grosso, Juan Pablo Tosar, Uciel Chorostecki, Silvana V Spinelli","doi":"10.3390/ncrna12010005","DOIUrl":"10.3390/ncrna12010005","url":null,"abstract":"<p><p><b>Background/Objectives:</b> Human milk is a complex biological fluid containing not only macro- and micronutrients but also diverse bioactive molecules, including extracellular RNAs. Although RNA has been detected in milk for decades, only a subset of RNA species has been characterized in detail, and abundant families such as tRNA-, yRNA-, and rRNA-derived fragments remain underexplored. This study aimed to define the composition, fragmentation patterns, stability, and exploratory functional activity of these highly abundant RNAs in human milk. <b>Methods:</b> We performed small RNA sequencing on skim milk samples and analyzed the resulting profiles in comparison with publicly available milk and biofluid datasets. RNA stability assays, Northern blotting, and RT-qPCR were conducted to validate RNA abundance and degradation kinetics. Extracellular vesicles (EVs) and non-vesicular fractions were analyzed to determine the subcellular distribution of RNA species. Exploratory functional assays using synthetic RNA fragments were carried out to assess their ability to modulate cellular responses in vitro. <b>Results:</b> Human milk was found to be highly enriched in small RNA fragments derived from tRNA, yRNA, and rRNA, dominated by a limited set of discrete sequences. These profiles were highly reproducible across independent datasets and distinct biofluids. Orthologal validation assays confirmed their abundance and stability, with RNA levels exceeding those of serum by over two orders of magnitude. Full-length transcripts were enriched in EVs, whereas shorter fragments predominated in the non-vesicular fraction. Synthetic milk-derived exRNAs showed detectable pro-survival activity under stress conditions in vitro. <b>Conclusions:</b> This study reveals that human milk carries a limited set of highly abundant stable sRNA molecules, primarily derived from tRNAs, yRNAs, and rRNAs. These findings provide new insights into the RNA cargo of human milk and offer preliminary evidence that selected sRNA fragments can modulate cellular stress responses in in vitro models.</p>","PeriodicalId":19271,"journal":{"name":"Non-Coding RNA","volume":"12 1","pages":""},"PeriodicalIF":4.2,"publicationDate":"2026-02-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12921927/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146258926","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanisms at the Intersection of lncRNA and m6A Biology.","authors":"Samuel J Gonzalez, Edgardo Linares, Allison M Porman Swain, Aaron M Johnson","doi":"10.3390/ncrna12010004","DOIUrl":"10.3390/ncrna12010004","url":null,"abstract":"<p><p>This review provides a thorough survey of long noncoding RNAs that bear the RNA modification N6-methyladenosine (m6A) and current work to understand the resulting mechanistic and biological consequences. We give an overview of lncRNA and m6A biology first, describing the writers, erasers, and readers of m6A and their targeting of lncRNAs. Next, we give an in-depth review of the field of nuclear lncRNAs that regulate chromatin and their regulation via m6A. We then describe the growing appreciation of liquid-liquid phase separation properties in lncRNA and m6A biology. Finally, we cover examples of cytoplasmic lncRNAs regulated by m6A. Overall, this review aims to emphasize how epitranscriptomics influences noncoding RNA mechanisms to provide additional layers of regulation, integrated into downstream biological processes.</p>","PeriodicalId":19271,"journal":{"name":"Non-Coding RNA","volume":"12 1","pages":""},"PeriodicalIF":4.2,"publicationDate":"2026-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12922158/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146257971","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hypercholesterolemia Impairs the Expression of Angiogenic MicroRNAs in Extracellular Vesicles Within Ischemic Skeletal Muscles.","authors":"Nozha Raguema, Sylvie Dussault, Kevin Sawaya, Michel Desjarlais, Eric Boilard, Sylvain Chemtob, Alain Rivard","doi":"10.3390/ncrna12010003","DOIUrl":"10.3390/ncrna12010003","url":null,"abstract":"<p><p><b>Background/Objectives</b>: In severe peripheral artery disease (PAD) with limb ischemia, hypercholesterolemia (HC) is associated with impaired neovascularization. Extracellular vesicles (EVs) are present within ischemic muscles, and they contain microRNAs (miRs) involved in several biological functions, including angiogenesis and neovascularization. <b>Methods</b>: We used a mouse model of PAD and compared the response to hindlimb ischemia in hypercholesterolemic ApoE<i>^-/-</i> vs. normocholesterolemic mice. Next-generation sequencing (NGS) was used to perform full miR expression profiling in ischemic skeletal muscles and in EVs of varying sizes-large EVs (lEVs) and small EVs (sEVs)-within these muscles. <b>Results</b>: We identified several miRs with potential pro-angiogenic effects (angiomiRs) that are reduced by HC in lEVs (Let-7b-5p, miR-151-3p, Let-7c-5p) or sEVs (miR-21a-5p, miR-196b-5p, miR-340-5p). As proof of principle, we showed that the overexpression of Let-7b-5p in lEVs, or miR-21a-5p in sEVs, can significantly increase the angiogenic capacity of these EVs in vitro. HC also impaired the enrichment of specific angiomiRs in lEVs (miR-100-5p), sEVs (miR-142a-3p), or in both lEVs and sEVs (miR-146b-5p). In silico approaches, including the prediction of miR targets, pathway unions, and gene unions, identified the resulting predictive effects of HC-modulated miRs in EVs on processes with key roles in the modulation of angiogenesis and neovascularization, such as the regulation of the actin cytoskeleton and focal adhesion and the HIF-1, MAPK, AMPK, and PI3K-Akt signaling pathways. <b>Conclusions</b>: Our results constitute an important first step towards the identification of specific miRs that could be targeted to improve EV angiogenic function in hypercholesterolemic conditions and reduce tissue ischemia in patients with severe PAD.</p>","PeriodicalId":19271,"journal":{"name":"Non-Coding RNA","volume":"12 1","pages":""},"PeriodicalIF":4.2,"publicationDate":"2026-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12922120/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146258966","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Role of microRNAs as Potential Biomarkers in Diffuse Large B-Cell Lymphoma.","authors":"Eirini Panteli, Epameinondas Koumpis, Vasileios Georgoulis, Georgios Petros Barakos, Evangelos Kolettas, Panagiotis Kanavaros, Alexandra Papoudou-Bai, Eleftheria Hatzimichael","doi":"10.3390/ncrna12010002","DOIUrl":"10.3390/ncrna12010002","url":null,"abstract":"<p><p>Diffuse large B-cell lymphoma (DLBCL) is the most common and clinically aggressive subtype of non-Hodgkin lymphoma (NHL). While novel therapies such as rituximab and polatuzumab vedotin have led to improved outcomes, approximately 35% of patients eventually develop relapsed or refractory disease. MicroRNAs (miRNAs), a class of endogenous single-stranded RNAs approximately 22 nucleotides in length, play a pivotal role in the regulation of gene expression at the post-transcriptional level through interactions with complementary target RNAs and contribute significantly to the development, progression, and treatment response of DLBCL. Oncogenic miRNAs, such as miR-155, miR-21, and the miR-17-92 cluster, promote proliferation, survival, immune evasion, and therapy resistance by modulating pathways including PI3K/AKT, NF-κB, and MYC. Conversely, tumor-suppressive miRNAs such as miR-34a, miR-144, miR-181a, and miR-124-3p inhibit oncogene activity and enhance apoptosis, with their loss often associated with adverse outcomes. Among these, miR-155 and miR-21 are particularly well studied, playing central roles in both tumor progression and remodeling of the tumor microenvironment. This review summarizes current evidence on the biological and clinical relevance of miRNAs in DLBCL, emphasizing their diagnostic and prognostic potential.</p>","PeriodicalId":19271,"journal":{"name":"Non-Coding RNA","volume":"12 1","pages":""},"PeriodicalIF":3.6,"publicationDate":"2026-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12821557/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146011219","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Functional and Molecular Characterization of Extracellular Vesicles Enriched in Exosomes Released by Bone Marrow Mesenchymal Stromal Cells Exposed to IFNγ in Combination with Autophagy Modulators Tamoxifen or Chloroquine.","authors":"Vladimir Beljanski, Maria J Moreno Hollweg, Renee Potens, Tanner Blaylock, Andres B Irausquin, Nikhila Paleati, Lubov Nathanson","doi":"10.3390/ncrna12010001","DOIUrl":"10.3390/ncrna12010001","url":null,"abstract":"<p><p><b>Background/Objectives</b>: Bone marrow mesenchymal stromal cells (MSCs) are therapeutic cells that adopt an immunomodulatory phenotype when exposed to pro-inflammatory cytokines. Recent research efforts uncovered that many therapeutic benefits of MSCs can be attributed to the secretion of extracellular vesicles (EVs) such as exosomes, small membrane vesicles of endocytic origin present in the cellular secretome. EVs' formation and release are impacted by the autophagy pathway, which recycles proteins and organelles via lysosomal degradation. <b>Methods</b>: To evaluate how modulation of autophagy affects properties of MSC EVs enriched in exosomes under pro-inflammatory conditions, we treated the cells with either tamoxifen (TX) or chloroquine (CQ), two drugs known to stimulate or inhibit autophagy, respectively, together with IFNγ. MSC EVs enriched in exosomes were then purified from serum-free media, and their immunoregulatory properties were evaluated ex vivo using activated CD4 T cells; small RNA sequencing was also conducted to determine EVs' microRNA content. <b>Results</b>: Our data indicate that MSCs treated with CQ + IFNγ yield EVs that possess somewhat higher capacity to decrease T cell proliferation compared to other EVs. Small RNA sequencing revealed that, although similar microRNAs were found in EVs isolated from all treated cells, the treatments exerted more effect on the levels of multiple microRNAs that are known to regulate either cancer or inflammation-related biological pathways in target cells. <b>Conclusions</b>: Overall, we conclude that the co-treatment of MSCs with TX or CQ in the presence of pro-inflammatory cytokine IFNγ has the potential to modulate microRNA content of EVs, potentially affecting biological properties of such EVs and their effect on target cells.</p>","PeriodicalId":19271,"journal":{"name":"Non-Coding RNA","volume":"12 1","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12821535/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146011245","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Transposable Element-Derived miR-28-5p and miR-708-5p: Exploring Potential Roles in Lung Cancer.","authors":"Sergiu Chira, Cornelia Braicu, Stefan Strilciuc, George A Calin, Ioana Berindan-Neagoe","doi":"10.3390/ncrna11060081","DOIUrl":"10.3390/ncrna11060081","url":null,"abstract":"<p><p><b>Background:</b> Transposable elements are normally silenced by epigenetic mechanisms; however, during malignant transformation, epigenetic alterations enable transposons to produce functional molecules like miRNAs. Among these, LINE-2 (L2) elements can generate miRNAs capable of regulating key genes, including tumor suppressors. Two L2-derived miRNAs, miR-28 and miR-708, have been linked to lung cancer, yet the mechanisms underlying their dysregulation remain poorly understood. Our study reveals how genomic context contributes to aberrant gene expression through comprehensive bioinformatic analyses. <b>Methods:</b> Using bioinformatics analysis, we evaluated the expression of miR-28 and miR-708 in lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC) datasets from TCGA. Further, we assessed the expression and methylation status of miR-28 and miR-708 host genes, <i>LPP</i> and <i>TENM4</i>, respectively, using computational tools. Finaly, we searched for potential candidate tumor suppressor genes targeted by miR-28 and miR-708, which are downregulated in LUAD and LUSC. <b>Results:</b> We found that intragenic L2-derived miR-28 and miR-708 are significantly upregulated in LUAD and LUSC. While <i>TENM4</i> gene also displays a marked increase in expression in LUAD and LUSC, in tumor versus normal tissue, this difference is less obvious for the <i>LPP</i> gene. We suggest that such dysregulations in expression might be linked to specific methylation patterns of their genomic locations. Furthermore, we emphasize that miR-28 and miR-708 might contribute to lung cancer pathogenesis by targeting key tumor suppressor genes. <b>Conclusions:</b> Alterations in the methylation status of L2-miRNAs genomic loci might result in elevated levels of miRNAs and subsequent targeting of tumor suppressor genes with potential implications in lung cancer pathogenesis.</p>","PeriodicalId":19271,"journal":{"name":"Non-Coding RNA","volume":"11 6","pages":""},"PeriodicalIF":4.2,"publicationDate":"2025-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12736026/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145820049","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MicroRNAs in Breast Cancer Bone Metastasis Formation and Progression: An Overview on Recent Progress in This Research Field.","authors":"Margherita Puppo","doi":"10.3390/ncrna11060080","DOIUrl":"10.3390/ncrna11060080","url":null,"abstract":"<p><p>Bone metastasis is a common and severe complication in advanced stages of breast cancer (BC) that is characterised by limited treatment options and poor patient prognosis. MicroRNAs (miRNAs) are a large class of regulatory small non-coding RNAs (ncRNAs) expressed by cells. Moreover, miRNAs can be released by cells into the blood and lymphatic streams, acting as distant cell-to-cell communicators. Of note, miRNAs have pivotal roles in the metastatic progression of BC to bone. This review summarises the most recent findings on miRNAs and their mRNA targets in driving BC bone metastasis. Furthermore, the potential clinical uses of miRNAs as future therapeutic targets/agents or biomarkers for BC bone metastasis are discussed.</p>","PeriodicalId":19271,"journal":{"name":"Non-Coding RNA","volume":"11 6","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12735869/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145820410","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"<i>CARINH</i>, an Interferon-Induced LncRNA in Cancer and Inflammation.","authors":"Morgane Gourvest, Coen van Solingen","doi":"10.3390/ncrna11060079","DOIUrl":"10.3390/ncrna11060079","url":null,"abstract":"<p><p><i>CARINH</i> is an intriguing long noncoding RNA whose unique regulatory functions intersect the seemingly distinct processes of innate immunity and cancer development. Notably, <i>CARINH</i> is conserved across species, offering powerful experimental models for uncovering its mechanistic roles and physiological functions across diverse biological contexts. Stimulated by interferons and viral infections, <i>CARINH</i> stands out as a key player in the body's antiviral defense mechanisms. Additionally, its dysregulation has been implicated in autoimmune disorders such as psoriasis, asthma, and inflammatory bowel disease, underscoring its broader role in maintaining immune homeostasis. Furthermore, alterations in <i>CARINH</i> expression have been connected to cancer progression, highlighting its dual role in immune response and tumor suppression. In this review, we delve into <i>CARINH</i>'s pivotal function in modulating interferon responses and influencing cancer development, with a focus on the molecular pathways that regulate its expression and contribute to its diverse roles. Understanding these pathways is crucial for evaluating <i>CARINH</i>'s significance as a biomarker and therapeutic target, potentially leading to groundbreaking advancements in medical research and treatment strategies.</p>","PeriodicalId":19271,"journal":{"name":"Non-Coding RNA","volume":"11 6","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12642018/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145588304","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}