Analytical Cellular Pathology最新文献

{"title":"Machine Learning-Based Text Processing Reveals Research Trends in Heterotopic Ossification.","authors":"Yangbai Sun, Qinyuan Zhu, Chaoran Yu, Chunmeng Wang, Wangjun Yan, Chaoyin Jiang","doi":"10.1155/ancp/9959615","DOIUrl":"10.1155/ancp/9959615","url":null,"abstract":"<p><strong>Background: </strong>Heterotopic ossification (HO) represents a highly active research field in pathological bone formation. Despite substantial advancements, a comprehensive understanding of its underlying mechanisms and clinical trajectory remains incomplete.</p><p><strong>Materials and methods: </strong>A bibliometric and machine-learning latent Dirichlet allocation (LDA) analysis was performed using data retrieved from the Web of Science Core Collection database.</p><p><strong>Results: </strong>A total of 4722 publications related to HO were identified. The most prolific countries included the USA, CHINA, GERMANY, the UK, JAPAN, SOUTH KOREA, ITALY, TURKEY, FRANCE, and CANADA . GERMANY demonstrated the highest citation strength, followed by CHINA . Aside from \"heterotopic ossification,\" other frequently occurring author keywords included \"fibrodysplasia ossificans progressive,\" \"complications\" and \"total hip arthroplasty.\" In keywords plus, besides HO, replacement, bone-formation, and arthroplasty were the most frequently occurring terms. Institutional network analysis with subject-specific clustering indicated that Shanghai Jiao Tong University was significantly enriched in radiology, nuclear medicine and medical imaging, while Wilderness Spine Serv specialized in surgical management. A developmental timeline plot of a network of most contributing authors also was visualized, along with the most influential references. Meanwhile, citation analysis indicated that Kaplan FS and Shore EM were the top-cited authors. By LDA analysis, a total of 16 key topics were identified in this field with distinct period-proportion visualization. One of the topics, cell bone express differentiation and formation has clearly dominated the last 10 years.</p><p><strong>Conclusion: </strong>This study constitutes the most extensive text processing analysis of HO to date, offering valuable insights and directions for future development.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2026 1","pages":"e9959615"},"PeriodicalIF":2.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13373702/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148457606","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":"Diagnostic Accuracy Rate of Tertiary Center Colposcopy Unit.","authors":"Emre Sertel","doi":"10.1155/ancp/9307280","DOIUrl":"10.1155/ancp/9307280","url":null,"abstract":"<p><strong>Introduction: </strong>Colposcopy plays a central role in the evaluation of cervical intraepithelial lesions; however, its diagnostic performance varies widely. While high sensitivity is desirable, low specificity may lead to unnecessary excisional procedures. This study aimed to evaluate the diagnostic performance of colposcopy and its potential contribution to overtreatment in a tertiary referral center.</p><p><strong>Methods: </strong>This retrospective single-center study included 150 patients who underwent LEEP between April 2023 and September 2024. Colposcopic impressions were compared with LEEP histopathological outcomes. Sensitivity, specificity, accuracy, positive predictive value (PPV), negative predictive value (NPV), and likelihood ratios were calculated. A subgroup analysis was performed for HPV16-positive patients.</p><p><strong>Results: </strong>Colposcopy demonstrated high sensitivity (93.9%, 95% CI: 87.3-97.4) but low specificity (31.4%, 95% CI: 20.2-45.0), with an overall accuracy of 72.7% (95% CI: 65.0-79.2). The PPV and NPV were 72.6% (95% CI: 64.2-79.7) and 72.7% (95% CI: 51.9-86.9), respectively. The positive and negative likelihood ratios were 1.37 and 0.19. Notably, 35 patients (23.3%) were false positives. In HPV16-positive patients, sensitivity was 80.8% (95% CI: 71.7-87.5), specificity was 33.3% (95% CI: 21.9-47.1), and accuracy was 64.7% (95% CI: 56.7-72.0).</p><p><strong>Conclusion: </strong>Although colposcopy is highly sensitive, its low specificity may result in substantial overtreatment, particularly in tertiary referral settings.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2026 1","pages":"e9307280"},"PeriodicalIF":2.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13255002/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148220613","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":"CCDC97 is a Promising Predictor in Cancer Diagnosis: A Pan Cancer Analysis.","authors":"Changye Yang, Ruirui Yang, Rundong Wang, Guo Ma, Lixin Hua","doi":"10.1155/ancp/2230769","DOIUrl":"10.1155/ancp/2230769","url":null,"abstract":"<p><strong>Background: </strong>Coiled-coil domain-containing 97 (CCDC97) can bind to the splicing factor SF3B complex to participate significantly in pre-mRNA splicing. However, there may be a risk of cancer development in the case of disrupted mechanism, necessitating further in-depth investigation of the underlying mechanism.</p><p><strong>Methods: </strong>The present study was conducted by searching for various databases to implement a comprehensive cancer analysis of CCDC97. Furthermore, a competitive endogenous RNA (ceRNA) network of CCDC97 was established, which was further integrated with the reported oncogene mechanisms in the CCDC family to explain the potential reasons for its abnormal expression.</p><p><strong>Results: </strong>CCDC97 is highly expressed in various cancers and closely associated with poor prognosis. CCDC97 was also strongly associated with the infiltration of various immune cells and multiple immune checkpoints in the tumor immune microenvironment. RT-qPCR showed that CCDC97 was highly expressed in hepatocellular carcinoma (HCC) tissue samples. At the single-cell level, CCDC97 exhibited an intimate association with depleted T cells in HCC tissues.</p><p><strong>Conclusion: </strong>In cancers, particularly in HCC CCDC97 can serve as a promising marker for immunotherapy and prognosis in cancers, particularly in HCC. More experimental verification is needed in the future research.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2026 1","pages":"e2230769"},"PeriodicalIF":2.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13580819/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147437226","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":"How the Fibrotic Lung Microenvironment Regulates Stem Cell Behavior: Immune Cues, Extracellular Matrix Remodeling, and Therapeutic Implications.","authors":"Zihan Zhou, Shuhua Han, Yuanfang Duan, Minqi Hong, Jie Huang","doi":"10.1155/ancp/1319659","DOIUrl":"10.1155/ancp/1319659","url":null,"abstract":"<p><p>Pulmonary fibrosis (PF) is a chronic and progressive interstitial lung disease characterized by excessive extracellular matrix (ECM) deposition and remodeling of lung structures. Currently, no effective clinical treatments exist to reverse or halt the progression of PF. Consequently, there is an urgent need to identify novel therapeutic strategies for this complex disease. Stem cells, renowned for their self-renewal and multipotent differentiation capabilities, have garnered considerable attention for their potential therapeutic applications, particularly in regenerative medicine. The primary stem cell types investigated for PF treatment include mesenchymal stem cells (MSCs), induced pluripotent stem cells (iPSCs), and lung progenitor cells. Preclinical studies have demonstrated that these stem cells can reduce inflammation, modulate immune responses, and promote the repair of damaged lung tissue. Although stem cell transplantation shows promise in PF treatment, challenges such as safety, quality control, and therapeutic efficacy remain unresolved. Recent studies have highlighted that stem cells interact with and modify their transplanted environment, influencing their structural properties and chemical composition. These interactions strongly influence stem cell survival, phenotype, and therapeutic efficacy. Understanding these dynamics will inform the development of new strategies to improve the effectiveness of stem cell therapies for PF.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2026 1","pages":"e1319659"},"PeriodicalIF":2.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13580849/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147437152","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":"AC104024.2/miR-30a-5p Axis Regulates Malignant Progression of Breast Cancer Through a Depression-Related Gene, MAP2K3.","authors":"Jun Li, Jie Sun, Lili Jiang, Xue Bai, Jiyue Gao, Zuowei Zhao","doi":"10.1155/ancp/6608116","DOIUrl":"https://doi.org/10.1155/ancp/6608116","url":null,"abstract":"<p><strong>Background: </strong>Breast cancer (BC), a malignant tumor, is characterized by high incidence and poor prognosis among women worldwide. Long noncoding RNAs (lncRNAs) and microRNAs (miRNAs) can regulate the initiation and progression of BC through competitive endogenous RNA (ceRNA) mechanisms. Despite depression being an important factor affecting patients with BC, the ceRNA regulatory network involving depression-related genes in BC remains unclear.</p><p><strong>Methods: </strong>In this study, we explored the role of the AC104024.2/miR-30a-5p axis in BC progression by targeting the depression-related gene mitogen-activated protein kinase kinase 3 (MAP2K3). We used depression-like mouse models to confirm the role of MAP2K3 in modulating depressive behavior. Additionally, gene set enrichment analyses (GSEA) and phenotypic experiments were conducted to verify the effects of the AC104024.2/miR-30a-5p/MAP2K3 axis on BC cell proliferation, migration, and apoptosis. Luciferase reporter assays were performed to demonstrate the ceRNA function of AC104024.2 for miR-30a-5p.</p><p><strong>Results: </strong>Our results showed that the AC104024.2/miR-30a-5p axis promotes the malignant progression of BC by regulating MAP2K3. In depression-like mouse models, MAP2K3 was identified as a key gene modulating depressive behavior. The AC104024.2/miR-30a-5p/MAP2K3 axis significantly influenced BC cell proliferation, migration, and apoptosis. Luciferase reporter assays confirmed that AC104024.2 acts as a ceRNA for miR-30a-5p, thereby affecting MAP2K3 expression. Rescue experiments suggested that the regulatory effects of AC104024.2 on BC malignancy are at least partly dependent on MAP2K3.</p><p><strong>Conclusion: </strong>This study uncovered the role of the depression-related ceRNA network in BC progression and identified AC104024.2 and MAP2K3 as potential biomarkers for the diagnosis and treatment of BC. These findings provide significant clinical implications and applications for the management of BC.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2026 1","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13691419/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149276239","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":"Deciphering HPV-Associated Immune Evasion in Cervical Cancer Through Multi-Omics Profiling and Computational Screening.","authors":"Rui Guo, Wenting He, Xia Liu, Na Zhang","doi":"10.1155/ancp/6756766","DOIUrl":"10.1155/ancp/6756766","url":null,"abstract":"<p><strong>Background: </strong>Human papillomavirus (HPV) infection is a major contributor to cervical cancer (CC), yet the molecular mechanisms driving HPV-associated immune evasion remain largely undefined.</p><p><strong>Methods: </strong>Bulk RNA-seq (The Cancer Genome Atlas [TCGA]-CESC) and single-cell RNA-seq datasets (GSE171894, GSE197461) were analyzed to elucidate transcriptional and immune landscape differences between HPV-positive and HPV-negative cervical tumors. Differentially expressed genes (DEGs) were identified using DESeq2. Functional enrichment analyses were conducted through gene set enrichment analysis (GSEA), gene ontology (GO), and Kyoto Encyclopedia of Genes and Genomes (KEGG) methodologies. Immune evasion feature genes were selected employing LASSO, Random Forest, and SVM-RFE techniques. Regulatory networks for transcription factors and miRNAs were constructed. Immune infiltration was evaluated using CIBERSORT and ssGSEA. Validation of key signature genes was performed in CC cell lines (HeLa, SiHa, C33A, and W12) via real-time quantitative polymerase chain reaction (RT-qPCR) and Western blot. The functional roles of IFNGR1 were examined through siRNA-mediated knockdown, complemented by CCK-8, colony formation, Transwell migration/invasion, and flow cytometry apoptosis assays.</p><p><strong>Results: </strong>A total of 6266 DEGs effectively differentiated HPV-positive from HPV-negative tumors. HPV-positive tumors exhibited enrichment in viral infection and immune response pathways, while HPV-negative tumors demonstrated activation of oncogenic signaling. Machine learning algorithms identified IFNGR1, TRADD, and PSMB9 as immune evasion feature genes associated with HPV. Regulatory network analysis emphasized IRF1/IRF2 and several miRNAs as critical modulators. Immune infiltration analysis indicated increased infiltration of Dendritic and Plasma cells in HPV-positive tumors, correlating with TRADD expression. Kaplan-Meier analysis further showed a trend toward worse overall survival among HPV-positive patients with high IFNGR1 expression (hazard ratio [HR] = 1.78, 95% confidence interval [CI]: 0.86-3.68; log-rank p = 0.113). Notably, IFNGR1 was significantly upregulated in HPV-positive CC cell lines at both mRNA and protein levels. IFNGR1 knockdown markedly inhibited proliferation, colony formation, migration, and invasion, while enhancing apoptosis in HeLa and SiHa cells, thereby confirming its essential role in the progression of HPV-associated CC.</p><p><strong>Conclusion: </strong>This study identified IFNGR1 as a key immune evasion-related gene in HPV-positive CC, elucidating its regulatory network and functional contributions, while positioning it as a potential therapeutic target for HPV-associated tumors.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2026 1","pages":"e6756766"},"PeriodicalIF":2.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13501396/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148809218","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":"Ophiopogonin D Alleviates Nonalcoholic Steatohepatitis via Ferroptosis Through AKT1/STAT3/HIF-1α Axis.","authors":"Dong Li, Meina Shi, Zhike Fang, Xiaoqing Wang, Linshi Huang, Mingguo Dong","doi":"10.1155/ancp/5567109","DOIUrl":"10.1155/ancp/5567109","url":null,"abstract":"<p><strong>Background: </strong>Not enough is known about how ophiopogonin D (OP-D) works and the molecular mechanisms involved in nonalcoholic steatohepatitis (NASH). This study aimed to investigate the antifibrosis effect and underlying mechanism of OP-D in NAFLD.</p><p><strong>Methods: </strong>The rats were fed a high-fat diet (HFD) to simulate NAFLD. After OP-D treatment or not, the rat serum lipid levels and inflammatory and ferroptosis-related factors were detected. Online databases and network pharmacology were used to collect the targets of OP-D against NASH. The effect of OP-D on AKT1, STAT3, ferroptotic markers, and fibrotic markers was determined using western blot or PCR assays.</p><p><strong>Results: </strong>OP-D inhibited abnormal liver function, fibrotic markers (α-SMA/Col1α1), and ferroptosis-related factor (GPX4) in NASH rats. Network pharmacology proposed AKT1 and STAT3 as targets for OP-D against NASH. OP-D reduced the p-AKT and p-STAT3 in liver tissues. OP-D reduced the levels of AKT1, STAT3, and HIF-1α in model hepatic stellate cells. AKT1 and STAT3 overexpression reversed the antifibrosis and ferroptosis-induced effects of OP-D in model hepatic stellate cells.</p><p><strong>Conclusion: </strong>OP-D may alleviate fibrosis in NASH by regulating ferroptosis via the AKT1/STAT3/HIF-1α axis.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2026 1","pages":"e5567109"},"PeriodicalIF":2.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13580853/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147505248","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":"CCND1 Stability Regulated by USP7 Deubiquitination Controls Glioma Radioresistance via Ferroptosis.","authors":"Yayu Zhuo, Chenrui Zhang, Xiaoyu Li, Zishuo Du, Yiren Rong, Di Zhang, Haijuan Mi, Xiaoyu Gu, Feng Wang, Haie Han, Jianliang Wu, Jianping Sun","doi":"10.1155/ancp/1041908","DOIUrl":"10.1155/ancp/1041908","url":null,"abstract":"<p><p>Dysregulation of Cyclin D1 (CCND1) is implicated in various cancers, but its specific contribution to glioma radioresistance and the associated regulatory mechanisms remain largely unexplored. This research aimed to elucidate the functional role and underlying mechanisms of CCND1 in glioma radioresistance. Our findings revealed that CCND1 is significantly upregulated in glioma tissues, which correlates with a poor prognosis. Furthermore, CCND1 knockdown inhibited proliferation, triggered apoptosis, and augmented radiosensitivity in glioma cells. Additionally, CCND1 depletion sensitized glioma cells to irradiation by driving ferroptosis, as indicated by elevated reactive oxygen species (ROS) production, lipid peroxidation, and intracellular Fe²⁺ accumulation. Mechanistically, USP7 was identified to stabilize the CCND1 protein via K48-linked deubiquitination. Notably, the ectopic expression of USP7 reversed the impacts of CCND1 knockdown on radiosensitivity, ferroptosis, cellular proliferation, and apoptosis. Altogether, our data indicate that the stabilization of CCND1 mediated by USP7 promotes radioresistance in glioma by suppressing ferroptosis. Therefore, targeting USP7 may serve as a promising therapeutic approach to augment the efficacy of radiotherapy in glioma.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2026 1","pages":"e1041908"},"PeriodicalIF":2.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13576636/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148971935","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":"RPARP-AS1 Targets miR-10b-5p to Influence Prognosis in Non-Small Cell Lung Cancer and Inhibit Tumor Progression.","authors":"Conghui Wang, Jing Zhang, Xin Wang, Jianzhu Yang, Zhenlong Zhu, Ruoshi Yuan, Duojun Qiu","doi":"10.1155/ancp/8817867","DOIUrl":"10.1155/ancp/8817867","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the roles of RPARP-AS1 and miR-10b-5p in regulating the prognosis and tumor progression of non-small cell lung cancer (NSCLC).</p><p><strong>Methods: </strong>A total of 138 NSCLC patients were enrolled. Surgical specimens were stored in liquid nitrogen. All patients received 5 years of clinical follow-up for prognostic assessment. In addition, multivariate Cox regression analysis was conducted to identify independent factors affecting NSCLC prognosis, and gene expression levels were quantified by reverse transcription quantitative polymerase chain reaction (RT-qPCR). Cell Counting Kit-8 (CCK-8) assays were performed to examine cell proliferation, and transwell assays were used to assess cell migration and invasion. Furthermore, nuclear-cytoplasmic fractionation experiments were conducted to localize RPARP-AS1 distribution. The interaction between RPARP-AS1 and miR-10b-5p was examined by dual luciferase reporter assays, and downstream targets in NSCLC were predicted using databases.</p><p><strong>Results: </strong>RPARP-AS1 was downregulated, while miR-10b-5p was upregulated in both NSCLC patient tissues and cells. Patients with reduced RPARP-AS1 expression or increased miR-10b-5p expression had lower survival rates, accompanied by worsened tumor size, differentiation, and metastasis. oe-RPARP-AS1 inhibited tumor cell proliferation, migration, and invasion. However, RPARP-AS1-induced functional alterations in NSCLC cells were mediated by miR-10b-5p. A total of 47 overlapping genes were identified to potentially mediate downstream signaling pathways of the RPARP-AS1/miR-10b-5p axis in NSCLC cells.</p><p><strong>Conclusion: </strong>Silencing RPARP-AS1 targeted miR-10b-5p to induce NSCLC cell proliferation, migration, and invasion, leading to tumor progression and poor prognosis.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2026 1","pages":"e8817867"},"PeriodicalIF":2.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13639925/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149117174","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":"RETRACTION: Sevoflurane Ameliorates Myocardial Cell Injury by Inducing Autophagy via the Deacetylation of LC3 by SIRT1.","authors":"Analytical Cellular Pathology","doi":"10.1155/ancp/9862018","DOIUrl":"10.1155/ancp/9862018","url":null,"abstract":"","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2026 1","pages":"e9862018"},"PeriodicalIF":2.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13253604/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148220570","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}