{"title":"Hsa_circ_0000140 Mediates the Regulation of Retinal Microvascular Endothelial Function and Inflammation via Sponging miR-485-5p in Diabetic Retinopathy.","authors":"Ting Feng, Ting Yan, Tanwei Wei, Si Cao, Huan Nie","doi":"10.1111/apm.70212","DOIUrl":"10.1111/apm.70212","url":null,"abstract":"<p><p>Diabetic retinopathy (DR), an ocular disease resulting from retinal microvascular damage caused by diabetes, has circular RNAs playing a key regulatory role in its progression. We examine the involvement of hsa_circ_0000140 in DR progression and its molecular regulation. We evaluated hsa_circ_0000140 and miR-485-5p expression in DR clinical samples and retinal endothelial cells with RT-qPCR. Diagnostic utility was examined by ROC curve analysis. Dual luciferase assays validated the targeting interaction, while proliferation was characterized using CCK-8, migration by Transwell, and inflammatory cytokines by ELISA. Elevated levels of hsa_circ_0000140 in DR patient serum and high-glucose-treated hRMECs indicate its diagnostic potential. Functionally, this molecule enhances cell proliferation, migration, and inflammatory cytokine release. It directly targets miR-485-5p, showing an inverse correlation with this microRNA. Restoring miR-485-5p expression counteracted these pathological processes, whereas hsa_circ_0000140 overexpression suppressed miR-485-5p function. Furthermore, miR-485-5p directly bound OGT, a gene highly expressed in DR. Hsa_circ_0000140 shows promise as a DR diagnostic marker and contributes to disease progression through miR-485-5p targeting, influencing retinal vascular function and inflammatory responses.</p>","PeriodicalId":8167,"journal":{"name":"Apmis","volume":"134 5","pages":"e70212"},"PeriodicalIF":2.2,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147832880","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Familial Adenomatous Polyposis-Risk of Cancer, Cancer Prevention, and Long-Term Consequences: Learnings from Five Decades with the Danish Polyposis Register.","authors":"John Gásdal Karstensen","doi":"10.1111/apm.70191","DOIUrl":"10.1111/apm.70191","url":null,"abstract":"<p><p>Familial adenomatous polyposis (FAP) is a hereditary condition marked by the growth of hundreds to thousands of adenomatous polyps in the colon and rectum, significantly elevating the risk of colorectal cancer (CRC) if left untreated. Caused by pathogenic variants in the APC gene, FAP is typically identified in adolescence, often leading to the recommendation of prophylactic colectomy to reduce the risk of CRC. However, even with colectomy, FAP patients face higher risks for other cancers, notably in the duodenum and pancreas. Our studies emphasize the importance of lifelong endoscopic surveillance and tailored treatment strategies to detect and manage precancerous lesions in the gastrointestinal tract. Advances in genetic screening have also significantly improved early detection and family risk management, especially for at-risk relatives. The Danish Polyposis Register, for example, is a comprehensive, nationwide database enabling tracking and preventative care for FAP families, effectively prolonging life expectancy by facilitating early intervention and surveillance of cancer risks. Endoscopic evaluation may differentiate between classical FAP and attenuated FAP (AFAP), a milder form with fewer polyps and a delayed onset, although both types require consistent monitoring due to elevated cancer risks. Innovations in genetic research, including the use of whole-genome sequencing, continue to refine risk assessments, helping to prevent unnecessary surgical interventions while providing personalized management plans for each patient. The disease's impact extends beyond physical health; the hereditary nature of FAP leads to psychological stress, often resulting in higher anxiety, depression, and educational challenges among patients. Adolescents and young adults, in particular, might benefit from targeted psychological support and educational interventions to help manage the mental and social implications of living with a chronic, cancer-prone condition. Studies underscore the need for interdisciplinary care to support these aspects of patients' lives, as they face unique challenges not experienced by other populations. Overall, research suggests that FAP treatment must integrate comprehensive cancer surveillance, proactive genetic screening, mental health support, and tailored medical interventions. The success of multidisciplinary, national registers like Denmark's emphasizes the importance of such models worldwide and should encourage the development of similar programs to improve patient outcomes and support those at high risk for hereditary cancers.</p>","PeriodicalId":8167,"journal":{"name":"Apmis","volume":"134 5","pages":"e70191"},"PeriodicalIF":2.2,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13155487/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147855769","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Hsa-Let-7c-3p Inhibits Retinoblastoma Cell Growth and Metastasis and Induces Pyroptosis by Targeting ARHGAP11A.","authors":"Qian Liu, Yuanyuan Li, Ping Chen, Na Liu","doi":"10.1111/apm.70213","DOIUrl":"10.1111/apm.70213","url":null,"abstract":"<p><p>Retinoblastoma (Rb) is a malignant intraocular tumor commonly seen in infants and young children, whose exact cause is unknown. This study aimed to investigate the molecular mechanisms affecting Rb progression. Hsa-let-7c-3p and ARHGAP11A were screened by bioinformatics. RT-qPCR and western blotting were used to detect the expression of hsa-let-7c-3p and ARHGAP11A, and their targeting relationship was examined by a dual luciferase reporter assay. Transwell or CCK-8 was used for cell invasion or viability evaluation. Pyroptosis was evaluated by detecting caspase-1 activity, cleaved GSDMD expression, and IL-1β/IL-18 secretion. The receiver operating characteristic (ROC) curve and binary logistic regression model were used to evaluate the diagnostic value of hsa-let-7c-3p/ARHGAP11A in Rb. Hsa-let-7c-3p was downregulated in Rb cells, and it inhibited ARHGAP11A expression by binding to its mRNA. Overexpression of ARHGAP11A intensified the malignant phenotypes of Rb cells and reversed the growth/invasion inhibition and pyroptosis promotion induced by hsa-let-7c-3p upregulation. Hsa-let-7c-3p and ARHGAP11A were the factors influencing Rb, and their combination showed higher accuracy in diagnosing Rb (AUC = 0.905) compared with single-factor prediction. In conclusion, Hsa-let-7c-3p suppressed Rb cell proliferation/invasion and induced pyroptosis by negatively regulating ARHGAP11A. They are potential biomarkers of Rb.</p>","PeriodicalId":8167,"journal":{"name":"Apmis","volume":"134 5","pages":"e70213"},"PeriodicalIF":2.2,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147986381","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Breaking the Barrier: Cutting-Edge Microbial Strategies Against Candida Biofilm Infections.","authors":"Utkalika Mallick, Binaya Krushna Sahu, Sudipta Kumar Patra, Mahesh Chandra Sahu, Sujogya Kumar Panda","doi":"10.1111/apm.70214","DOIUrl":"10.1111/apm.70214","url":null,"abstract":"<p><p>Candida species, particularly Candida albicans and nonalbicans, can form strong biofilms on biotic and abiotic surfaces, leading to chronic and recurring infections. These biofilms are influenced by regulatory circuits, transcription factors, and morphogenetic changes that promote biofilm development and drug resistance. The biofilm matrix, including β-glucans and extracellular DNA, hinders antifungal penetration. Next-generation approaches to controlling Candida biofilms include small-molecule inhibitors, quorum-sensing inhibitors, enzyme-based ECM inhibitors, and nanoparticle-mediated drug delivery platforms. Marine-derived metabolites, antimicrobial peptides, and monoclonal antibodies are also discussed for their antibiofilm activity. Innovative in vitro and in vivo models are presented for assessing biofilm behavior and treatment response. Polymicrobial biofilms, including Candida and bacteria, are also discussed. Obstacles to controlling Candida biofilms include antifungal resistance, therapeutic agent toxicity, and regulatory hurdles. Future directions include CRISPR-based gene editing, antifungal vaccines, and omics-based target identification. This review emphasizes the importance of multidisciplinary, biofilm-centric therapeutic strategies in reducing the global health impact of Candida biofilm-related infections and advancing innovative antifungal therapies.</p>","PeriodicalId":8167,"journal":{"name":"Apmis","volume":"134 5","pages":"e70214"},"PeriodicalIF":2.2,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147760270","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}