Huirong Yan, Qingshuang Qin, Yanling Li, Li Yang, Mingjuan Jiang, Yujie Xin, Yu Li, Xiaoyang Li, Jianhong Lu
{"title":"Multiomics analyses identify diet-derived creatine and α-linolenic acid linking with metastatic thyroid cancer.","authors":"Huirong Yan, Qingshuang Qin, Yanling Li, Li Yang, Mingjuan Jiang, Yujie Xin, Yu Li, Xiaoyang Li, Jianhong Lu","doi":"10.1016/j.mcp.2026.102086","DOIUrl":"https://doi.org/10.1016/j.mcp.2026.102086","url":null,"abstract":"<p><strong>Background: </strong>Thyroid cancer (TC) has traditionally been regarded as an indolent malignancy. However, it retains the potential for metastasis and lethality, underscoring its status as a malignant tumor. To explore the interplay between serum metabolite profiles, gut microbial communities, and TC metastasis, we conducted a comprehensive study.</p><p><strong>Methods: </strong>Serum metabolites were analyzed using untargeted metabolomics methods to characterize the metabolic changes. Two diet-derived metabolites, creatine (Cr) and α-linolenic acid (ALA), were selected for in vitro validation. Finally, 16S rRNA gene sequencing was used to characterize the intestinal microbial composition and analyze the correlation between differential metabolites and differential intestinal microbiota.</p><p><strong>Results: </strong>LC-MS analysis of serum metabolites identified Arginine and proline metabolism and Arginine biosynthesis as the primary metabolic pathways altered in TC metastasis. Both Cr and ALA effectively inhibited EMT, migration, and invasion of TC cell lines, TPC1 and FTC-133. The analysis of gut microbiota composition revealed that Cr and ALA showed significant correlations with the bacteria genera, Porphyromonas and Papillibacter.</p><p><strong>Conclusions: </strong>This study highlights that TC metastasis is associated with significant alterations in the serum metabolite profiles of patients, and Cr and ALA play a role in inhibiting TC development. Furthermore, Cr and ALA were correlated with Porphyromonas and Papillibacter, implying their potential link with food-borne components and their connected impact on TC metastasis. The findings provide new insights into the role of metabolites and gut microbiota in TC progression, suggesting novel avenues for dietary intervention in cancer treatment.</p>","PeriodicalId":49799,"journal":{"name":"Molecular and Cellular Probes","volume":" ","pages":"102086"},"PeriodicalIF":3.2,"publicationDate":"2026-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148892798","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Soluble PD-1/PD-L1 biomarkers in NSCLC: prognostic and diagnostic value.","authors":"Konstantinos Vachlas, Chronis Fatouros","doi":"10.1016/j.mcp.2026.102087","DOIUrl":"10.1016/j.mcp.2026.102087","url":null,"abstract":"<p><strong>Background: </strong>Tissue-based immunohistochemistry (IHC) for programmed death-ligand 1 (PD-L1) remains the clinical standard for guiding immunotherapy selection in non-small cell lung cancer (NSCLC) but is constrained by intratumoral spatial heterogeneity and procedural sampling risks. Circulating soluble PD-1 (sPD-1) and soluble PD-L1 (sPD-L1) generated either through alternative mRNA splicing or by ADAM10/17-mediated proteolytic shedding offer minimally invasive liquid-biopsy alternatives that capture systemic immune dynamics in real time.</p><p><strong>Methods: </strong>This review synthesizes clinical and translational data from prospective validation cohorts, surgical trials, and multi-center meta-analyses to evaluate the stage-stratified diagnostic utility, prognostic reliability, and treatment-response predictive value of sPD-1 and sPD-L1 across diverse therapeutic contexts.</p><p><strong>Results: </strong>Cross-sectional baseline assessments show modest standalone diagnostic sensitivity due to significant absolute concentration overlaps between oncological cohorts and healthy controls. However, elevated pre-treatment sPD-L1 functions as a robust independent negative prognostic indicator of overall survival (OS) and a predictor of primary resistance to immune checkpoint inhibitors (ICIs) across advanced stages, while demonstrating no prognostic relevance under conventional cytotoxic chemotherapy. Longitudinally, an acute postoperative sPD-L1 increase of ≥20% at four months marks micro-metastatic persistence and predicts disease recurrence in early-stage surgical cohorts (Odds Ratio = 10.29). Conversely, sPD-1 demonstrates distinct stage-specific volatility; pre-treatment profiles lack stable prognostic indicators, but an early on-treatment plasma surge during anti-PD-1 monotherapy independently maps to prolonged progression-free survival and superior OS (Hazard Ratio = 0.24). Finally, composite liquid biosignatures (e.g., sCombo or joint bsPD-L1/MMP screening) significantly optimize predictive resolution over single-analyte measurements.</p><p><strong>Conclusions: </strong>Circulating sPD-L1 serves as a reliable negative indicator of therapeutic efficacy and surgical durability, whereas on-treatment tracking of sPD-1 captures protective host T-cell clonal reactivation. Cross-platform assay standardization and predefined cutoff validation remain essential thresholds before these liquid biomarkers can be implemented into standard clinical practice and thoracic surgery. Integrating these circulating checkpoints into high-throughput multi-omics platforms and AI-based analytics is a promising next step toward reproducible predictive signatures that could guide personalized treatment in thoracic oncology.</p>","PeriodicalId":49799,"journal":{"name":"Molecular and Cellular Probes","volume":" ","pages":"102087"},"PeriodicalIF":3.2,"publicationDate":"2026-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148882260","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Longfei Fan , Zhaoying Wang , Tao Tao , Dongdong Huang , Xiaoyun Tang , Rui Wang , Zhongqiang Qin , Bo Xie , Yi Tan
{"title":"Exosomal IGFALS as a prognostic biomarker in hepatocellular Carcinoma: Associations with immune infiltration and clinical outcomes","authors":"Longfei Fan , Zhaoying Wang , Tao Tao , Dongdong Huang , Xiaoyun Tang , Rui Wang , Zhongqiang Qin , Bo Xie , Yi Tan","doi":"10.1016/j.mcp.2026.102061","DOIUrl":"10.1016/j.mcp.2026.102061","url":null,"abstract":"<div><h3>Purpose</h3><div>This investigation seeks to examine the relationship between exosomal Insulin-like Growth Factor Binding Protein Acid Labile Subunit (IGFALS) gene expression, immune infiltration, and clinical outcomes in individuals with hepatocellular carcinoma (HCC).</div></div><div><h3>Method</h3><div>Clinical data and IGFALS expression levels were obtained from the TCGA and GEO databases. Immunohistochemistry was performed to confirm IGFALS expression in both HCC and adjacent non-tumor tissues. To validate survival analyses, restricted cubic spline models were used to explore associations between overall survival (OS) and the expression of IGFALS in liver hepatocellular carcinoma (LIHC). Gene set enrichment analysis (GSEA) identified IGFALS-associated pathways, while Gene set enrichment analysis (ssGSEA) evaluated IGFALS-immune cell infiltration correlations. Functional characterization included proliferation, migration/invasion, molecular profiling, and apoptosis assays.</div></div><div><h3>Result</h3><div>Compared to normal tissues, IGFALS expression levels were notably decreased in tumor tissues. A notable link was detected between IGFALS expression and multiple clinical factors, including gender, weight, residual tumor, adjacent hepatic tissue inflammation, vascular invasion, AFP, BCLC, tumor size, multinodular, TACE, and satellite lesion in HCC. Reduced IGFALS expression in HCC was correlated with decreased OS. Moreover, the IGFALS level in malignant tumor cells post-immunotherapy was observed to be markedly higher than that in the pre-treatment phase. A strong association between IGFALS and immune infiltration levels was also established. At the same time, in vitro experiments also verified the function of the IGFALS gene.</div></div><div><h3>Conclusion</h3><div>The exosomal IGFALS gene holds potential as a prospective indicator for assessing the outcome of individuals with HCC.</div></div>","PeriodicalId":49799,"journal":{"name":"Molecular and Cellular Probes","volume":"86 ","pages":"Article 102061"},"PeriodicalIF":3.0,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146047280","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Emerging roles of artificial intelligence/machine learning (AI/ML) towards new understandings in molecular crosstalk between circRNA–CUL3–TKI to resensitize chemoresistant cancers","authors":"Pranjali Dutta, Samiksha Middya, Siddharth Shome, Manshi Kumari Gupta, Poobana Dharmalingam, C. Sudandiradoss","doi":"10.1016/j.mcp.2026.102063","DOIUrl":"10.1016/j.mcp.2026.102063","url":null,"abstract":"<div><div>Cancer arises and is resistant to therapy via intricate molecular networks that are poorly characterised. While individually, Cullin-3 (CUL3) and circular RNAs (circRNAs) have been reported to modulate cancer, their synergistic effect in the modulation of tyrosine kinase inhibitor (TKI) resistance is yet to be studied. An emerging circRNA–CUL3–TKI regulatory framework is highlighted as a potential contributor to oncogenesis and drug sensitivity in this review. We discuss how circRNA-associated networks may influence CUL3-dependent pathways implicated in tumour resistance to therapy by modulating autophagy, ferroptosis, stress-responses, and redox signalling. Exosomal circRNAs and circRNAs of the CUL3 gene itself are highlighted as dynamic mediators of resistance as well as biomarkers. How they interact with Kelch-like ECH-associated protein 1- Nuclear factor erythroid 2-related factor 2 (KEAP1–NRF2) signalling reveals that they enhance tumour survival under therapy pressure. By highlighting key processes of carcinogenesis and resistance, the circRNA–CUL3–TKI axis represents a testable therapeutic framework. Modeling circRNA networks, predicting TKI response, finding biomarkers, and developing personalised treatment plans are all made possible by applications of artificial intelligence and machine learning (AI/ML), as explored in this review. Antisense oligonucleotides, Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR)-based molecules, neddylation inhibitors or PROteolysis TArgeting Chimera (PROTACs) are examples of potential interventions that, when combined with AI/ML techniques, improve therapeutic efficacy and may inform future desensitisation strategies. These collectively emphasize the emerging applications for AI/ML in understanding the circRNA–CUL3–TKI crosstalk and developing methods to resensitize cancers that are resistant to therapy.</div></div>","PeriodicalId":49799,"journal":{"name":"Molecular and Cellular Probes","volume":"86 ","pages":"Article 102063"},"PeriodicalIF":3.0,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146101023","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Metformin and oncogenic pathways: Crosstalk between energy sensing and tumor progression","authors":"Ying Zhang, Long Zhao, Kai Zhang, Yuqiu Gao","doi":"10.1016/j.mcp.2026.102068","DOIUrl":"10.1016/j.mcp.2026.102068","url":null,"abstract":"<div><div>Metformin, a widely prescribed oral biguanide for type 2 diabetes mellitus, has gained significant attention as a potential anti-cancer agent. Beyond its established role in improving insulin sensitivity and lowering blood glucose, preclinical and epidemiological studies suggest that metformin exerts anti-tumor effects through both insulin-dependent and insulin-independent mechanisms. Central to its activity is the activation of AMP-activated protein kinase (AMPK), which disrupts the mammalian target of rapamycin (mTOR) pathway, leading to cell cycle arrest, apoptosis, and reduced tumor growth. Additionally, metformin modulates oncogenic signaling networks such as PI3K/Akt, Erk, and receptor tyrosine kinases, while influencing tumor metabolism, angiogenesis, and immune responses. By inhibiting mitochondrial complex I, metformin interferes with cancer cell bioenergetics and the Warburg effect, further contributing to its anti-cancer potential. Clinical studies, however, have yielded mixed results, underscoring the complexity of metformin's effects and the need for rigorous investigation. This review highlights the multifaceted mechanisms by which metformin impacts tumor progression and discusses its promise and challenges as a therapeutic agent in cancer prevention and treatment.</div></div>","PeriodicalId":49799,"journal":{"name":"Molecular and Cellular Probes","volume":"86 ","pages":"Article 102068"},"PeriodicalIF":3.0,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146195477","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jie Shao , Xia Zheng , Lin Yang , Qian Yu , Zhichao Jin , Ran Yang , Zhanying Zhao , Borui Liu , Ruiping Wang , Mao Wang
{"title":"The role of WNT10B expression in the prognosis of colorectal cancer: A retrospective study based on TCGA database and clinical data","authors":"Jie Shao , Xia Zheng , Lin Yang , Qian Yu , Zhichao Jin , Ran Yang , Zhanying Zhao , Borui Liu , Ruiping Wang , Mao Wang","doi":"10.1016/j.mcp.2026.102062","DOIUrl":"10.1016/j.mcp.2026.102062","url":null,"abstract":"<div><h3>Objective</h3><div>To evaluate the prognostic value of WNT10B expression in colorectal cancer (CRC) for personalized management.</div></div><div><h3>Methods</h3><div>We analyzed a TCGA cohort of 644 CRC patients to assess differential expression of WNT family genes between 51 paired tumor-normal samples. Patients were stratified by WNT10B expression to compare overall survival (OS) and progression-free interval (PFI). Prognostic factors were identified via univariate and multivariate Cox regression. For validation, WNT10B protein expression was examined by immunohistochemistry in a separate cohort of 176 CRC patients who underwent surgery at our institution (2016–2020). Kaplan-Meier analysis and univariate Cox regression were used to correlate WNT10B levels with OS and disease-free survival (DFS).</div></div><div><h3>Results</h3><div>According to TCGA data, WNT10B was upregulated in CRC tumors. Elevated expression was correlated with reduced OS and PFI. Univariate analysis for OS implicated high WNT10B, age >65, lymph node/distant metastasis, positive margin, deep invasion, and abnormal CEA. For PFI, significant factors included high WNT10B, lymph node/distant metastasis, positive margin, deep invasion, and abnormal CEA. Multivariate analysis confirmed high WNT10B, age >65, and a positive margin as independent prognostic factors for OS. High WNT10B expression, distant metastasis, invasion depth and abnormal carcinoembryonic antigen level are the risk factors for independently predicting high tumor recurrence; Postoperative Kaplan-Meier analysis revealed that reduced WNT10B expression was associated with prolonged overall survival (OS), while disease-free survival (DFS) also tended to be longer in the low-expression group, although this trend did not reach statistical significance. Univariate Cox regression identified several factors adversely affecting OS, including elevated WNT10B expression, age ≥65 years, lymph node metastasis, distant metastasis, positive surgical margin, vascular invasion, and perineural invasion. Lymph node metastasis, distant metastasis, vascular invasion, and perineural invasion were also associated with increased recurrence risk. Multivariate analysis confirmed that age ≥65 years, distant metastasis, and vascular invasion were independent predictors of shorter OS. Distant metastasis emerged as an independent risk factor for tumor recurrence.</div></div><div><h3>Conclusion</h3><div>WNT10B is upregulated in colorectal cancer and correlates with unfavorable outcomes, suggesting its potential utility as a prognostic biomarker and therapeutic target.</div></div>","PeriodicalId":49799,"journal":{"name":"Molecular and Cellular Probes","volume":"86 ","pages":"Article 102062"},"PeriodicalIF":3.0,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147272676","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Xue Wang , Wenjun Wang , Ran Yao , Zhao Liu , Qianqing Wang
{"title":"Stem cell-derived and plant-derived exosomes: Promising therapeutics for skin healing and regeneration","authors":"Xue Wang , Wenjun Wang , Ran Yao , Zhao Liu , Qianqing Wang","doi":"10.1016/j.mcp.2026.102064","DOIUrl":"10.1016/j.mcp.2026.102064","url":null,"abstract":"<div><div>Stem cell-derived and plant-derived exosomes are emerging as promising therapeutic agents in cutaneous repair, regeneration, and rejuvenation. They facilitate wound healing and skin revitalization through multifaceted mechanisms, including immunomodulation, promotion of cellular differentiation, and stimulation of angiogenesis. Additionally, their ability to modulate collagen production and remodeling underscores their potential in addressing skin aging and improving cosmetic outcomes. Consequently, exosome-based therapies show promise for a range of conditions, from challenging wounds and skin aging to pigmentary disorders, hair loss, certain immune-mediated dermatoses. To ensure a comprehensive and unbiased synthesis of the current evidence, this systematic review was conducted following a structured methodology, encompassing a search across multiple major databases over a defined 20-year period. This review systematically outlines the roles and applications of commonly employed plant exosomes and stem cell exosomes in recent years' advancements in skin repair and cosmetic dermatology. By synthesizing the current understanding of their mechanisms and clinical potential, this review aims to highlight viable therapeutic strategies that bridge the gap between medical dermatology and aesthetic medicine.</div></div>","PeriodicalId":49799,"journal":{"name":"Molecular and Cellular Probes","volume":"86 ","pages":"Article 102064"},"PeriodicalIF":3.0,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146143777","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Reveal the regulatory role of DDX10 in diffuse large B-cell lymphoma: binding with FBL to promote cell proliferation and invasion","authors":"Xin Chen, Weiqing Chen","doi":"10.1016/j.mcp.2025.102057","DOIUrl":"10.1016/j.mcp.2025.102057","url":null,"abstract":"<div><h3>Background</h3><div>Diffuse large B cell lymphoma (DLBCL) is a heterogeneous malignancy with an unidentified molecular etiology. This study aims to investigate the role of DEAD-box helicase 10 (DDX10), a novel carcinogenic gene, in DLBCL.</div></div><div><h3>Methods</h3><div>The expression of DDX10 in DLBCL was analyzed by the GEPIA2 bioinformatics tool. DDX10 and fibrillarin (FBL) expressions in DLBCL patients’ cancer tissues and cell lines were measured via quantitative real-time reverse transcription polymerase chain reaction. RNA immunoprecipitation assay was used to confirm FBL-DDX10 interaction. The effects of DDX10/FBL overexpression and knockdown on cell viability, invasion, and Wnt/β-catenin pathway proteins were evaluated in DLBCL cell lines.</div></div><div><h3>Results</h3><div>DDX10 and FBL exhibited elevated expression levels in patients with DLBCL, particularly in those with stage III or IV DLBCL. DDX10 can bind to FBL in DLBCL cells. Silencing of DDX10 or FBL suppressed viability, proliferation and invasion, and downregulated the expressions of β-catenin, cyclin D1, and c-Myc proteins in DLBCL cells. The regulatory impact of DDX10 or FBL silencing on DLBCL cells was counteracted by the overexpression of FBL or DDX10.</div></div><div><h3>Conclusion</h3><div>DDX10 contributes to the proliferation and invasion of DLBCL cells via positively regulating FBL, highlighting the DDX10–FBL axis as a potential therapeutic target. This work provides new insights into DLBCL pathogenesis and underscores the biomedical relevance of targeting DDX10–FBL.</div></div>","PeriodicalId":49799,"journal":{"name":"Molecular and Cellular Probes","volume":"85 ","pages":"Article 102057"},"PeriodicalIF":3.0,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145665704","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Su Qin , Jing Zhang , Meifang Cao , Tao Jiang , Baohong Jiang
{"title":"Identification of lymphangiogenesis-related diagnostic model for predicting abdominal aortic aneurysm onset and progression and validation of lymphopoiesis in abdominal aortic aneurysm","authors":"Su Qin , Jing Zhang , Meifang Cao , Tao Jiang , Baohong Jiang","doi":"10.1016/j.mcp.2025.102054","DOIUrl":"10.1016/j.mcp.2025.102054","url":null,"abstract":"<div><div>This study aims to explore the lymphangiogenesis (LG)-related diagnostic markers of abdominal aortic aneurysm (AAA) through bioinformatics, as well as the alteration of the regional lymphatic system during the progression of AAA and the influence of lymphatic drainage obstruction on AAA progression. 2957 differentially expressed genes (DEGs) were identified between the AAA patient group and the healthy donor group in Gene Expression Omnibus microarray datasets. Subsequently, the DEGs and the LG gene were intersected, and 93 genes were obtained. Weighted gene co-expression network analysis (WGCNA) was performed to obtain module genes. Module genes intersected with the above 93 genes, and 26 genes were obtained. Five hub genes (HSPA5, RAB10, RAB1A, RAF1, SMAD4) identified by machine learning may serve as diagnostic candidates for AAA patients through nomogram and ROC evaluation. Gene set enrichment analysis (GSEA) and immune infiltration analysis were performed further to understand the function of these candidate genes and explore the effect of immunity in AAA, respectively. By establishing an AAA animal model, it was found that the iliac lymph nodes around the abdominal aorta were significantly enlarged, and the number and lumen size of lymphatic vessels in the vessel wall were both significantly increased during the progression of AAA. Additionally, AAA was significantly promoted by ligating lymphatic vessels, which caused lymphatic drainage obstruction around the abdominal aorta. Our findings have the potential to enhance knowledge about the development and diagnosis of AAA.</div></div>","PeriodicalId":49799,"journal":{"name":"Molecular and Cellular Probes","volume":"85 ","pages":"Article 102054"},"PeriodicalIF":3.0,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145439965","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}