Experimental and molecular pathology最新文献

{"title":"Antioxidant and neuroprotective effects of ubiquinol diacetate: Insights from SH-SY5Y cell line and Caenorhabditis elegans models of Parkinson's disease","authors":"Matteo Micucci ,&nbsp;Michela Battistelli ,&nbsp;Sabrina Burattini ,&nbsp;Riham Osman ,&nbsp;Francesco Onesimo ,&nbsp;Michele Mari ,&nbsp;Michele Retini ,&nbsp;Ilaria Versari ,&nbsp;Barbara Pagliarani ,&nbsp;Andrea Tarozzi ,&nbsp;Giovanni Zappia ,&nbsp;Federico Gianfanti ,&nbsp;Letizia Pruccoli","doi":"10.1016/j.yexmp.2026.105023","DOIUrl":"10.1016/j.yexmp.2026.105023","url":null,"abstract":"<div><div>Parkinson's disease (PD) is a neurodegenerative disease characterized by the degeneration of dopaminergic neurons in the substantia nigra and the presence of misfolded α-synuclein in the brain. Mitochondrial dysfunction and oxidative stress are factors contributing to the death of these neurons. Coenzyme Q10 (CoQ10) serve as an antioxidant and cofactor for mitochondrial enzymes, and its deficiency can exacerbate neurodegenerative processes in PD. However, the clinical efficacy of CoQ10 is limited by its low bioavailability and instability. Ubiquinol diacetate (CoQ10 Ac), an esterified form of CoQ10, shows improved pharmacokinetic properties and potential as a prodrug, converting into the reduced antioxidant form of CoQ10 by esterases in the body. This study aimed to investigate the antioxidant and neuroprotective effects of CoQ10 Ac compared to CoQ10 in SH-SY5Y cell line and <em>Caenorhabditis elegans</em> models of PD. CoQ10 Ac showed higher antioxidant activity than CoQ10 at both extracellular and intracellular levels, particularly in the membrane and cytosolic compartments. It exhibited superior neuroprotection against 6-hydroxydopamine toxicity, showing a greater ability to reduce the activation of caspase-3 and PARP1 compared to CoQ10. Both compounds decreased the increased ratio of mitochondrial fission protein, DRP1, to fusion protein, OPA1, induced by 6-hydroxydopamine in SH-SY5Y cells, enhancing OPA1 levels and promoting antiapoptotic death. However, CoQ10 Ac was more effective than CoQ10 in preserving mitochondrial structural integrity and mass. Additionally, both compounds significantly inhibited the aggregation of α-synuclein induced by 6-hydroxydopamine. Furthermore, CoQ10 Ac showed stronger neuroprotective effects than CoQ10 in <em>C. elegans</em> models of PD. It demonstrated greater anti-aggregant activity in <em>C. elegans</em> expressing human α-synuclein, suggesting higher bioavailability. These findings highlight CoQ10 Ac as a promising prodrug candidate and support further investigation in <em>in vivo</em> PD models.</div></div>","PeriodicalId":12176,"journal":{"name":"Experimental and molecular pathology","volume":"145 ","pages":"Article 105023"},"PeriodicalIF":3.7,"publicationDate":"2026-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145972767","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":"Exploring the characteristics of the SKP2-CDK6 axis in pancreatic cancer cell metastasis and its clinical significance","authors":"Hui-Ching Wang ,&nbsp;Chi-Wen Luo ,&nbsp;Sin-Hua Moi ,&nbsp;Ya-Hui Chang ,&nbsp;Shu-Jyuan Chang ,&nbsp;Yu-Hsuan Hung ,&nbsp;Tzu-Yi Chen ,&nbsp;Yi-Zi Chen ,&nbsp;Chiao-Ying Lai ,&nbsp;Yu-Ci Yang ,&nbsp;Chun-Chieh Wu ,&nbsp;Li-Tzong Chen ,&nbsp;Mei-Ren Pan","doi":"10.1016/j.yexmp.2026.105024","DOIUrl":"10.1016/j.yexmp.2026.105024","url":null,"abstract":"<div><h3>Background</h3><div>Pancreatic ductal adenocarcinoma (PDAC) is a highly metastatic malignancy with limited biomarkers for early detection. Recurrence and metastasis after surgical resection remain major causes of mortality, highlighting the urgent need for novel therapeutic strategies.</div></div><div><h3>Methods</h3><div>We integrated clinical database analyses and functional assays in PDAC cell lines and mouse models to investigate the role of the SKP2-CDK6 axis in tumor progression, metastasis, and gemcitabine resistance.</div></div><div><h3>Results</h3><div>Elevated CDK6 expression correlated with poorer progression-free and overall survival in PDAC patients and was associated with advanced stage and lymph node metastasis. SKP2 expression positively correlated with CDK6, and mechanistic studies revealed that SKP2 may transcriptionally regulate CDK6. Inhibition of CDK6 suppressed tumor growth and metastasis in vitro and in vivo, and reduced epithelial-mesenchymal transition. Combining a CDK6 inhibitor with gemcitabine significantly reduced colony formation in gemcitabine-resistant PDAC cells, suggesting a synergistic anticancer effect.</div></div><div><h3>Conclusions</h3><div>The SKP2-CDK6 axis may drive PDAC progression and chemoresistance. Co-targeting SKP2 and CDK6 in combination with gemcitabine may represent a promising therapeutic approach, warranting further preclinical and clinical evaluation to improve outcomes for patients with PDAC.</div></div>","PeriodicalId":12176,"journal":{"name":"Experimental and molecular pathology","volume":"145 ","pages":"Article 105024"},"PeriodicalIF":3.7,"publicationDate":"2026-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145972768","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":"Corrigendum to \"NVP-BEZ235 enhances autophagy and ameliorates cognitive deficits by targeting tauopathies\" [Experimental and Molecular Pathology 143 (2025) 104988].","authors":"Ifat Alsharif","doi":"10.1016/j.yexmp.2025.105018","DOIUrl":"https://doi.org/10.1016/j.yexmp.2025.105018","url":null,"abstract":"","PeriodicalId":12176,"journal":{"name":"Experimental and molecular pathology","volume":" ","pages":"105018"},"PeriodicalIF":3.7,"publicationDate":"2026-01-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145951719","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":"The role of myotubularin-related lipid phosphatases in cancer pathogenesis","authors":"Lenka Doubravská,&nbsp;Marie Macůrková","doi":"10.1016/j.yexmp.2026.105022","DOIUrl":"10.1016/j.yexmp.2026.105022","url":null,"abstract":"<div><div>Myotubularin-related proteins (MTMRs) comprise a family of lipid phosphatases using phosphatidylinositol 3-phosphate and phosphatidylinositol 3,5-bisphosphate as their substrate. Several members have a well-established role in the pathogenesis of human myopathies and neuropathies. There is a growing body of evidence that the portfolio of diseases where MTMRs play a role should be extended to cancer. MTMRs are thus closing the gap on their functional counterparts, the phosphatidylinositol kinases. MTMRs do not contribute to cancer initiation through driver mutations, but their expression in tumours is frequently altered, leading to defects in cell proliferation, migration or cell death. In some instances, MTMR misexpression contributes to resistance to cancer treatment. In this review we summarize the current knowledge with the emphasis on the molecular mechanisms underlying the MTMR function in cancer pathogenesis.</div></div>","PeriodicalId":12176,"journal":{"name":"Experimental and molecular pathology","volume":"145 ","pages":"Article 105022"},"PeriodicalIF":3.7,"publicationDate":"2026-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145911202","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":"Assessing the role of folate syntrophy and folate cross-feeding in the pathobiology of infectious-inflamed milieu caused by Fusobacterium nucleatum","authors":"Darab Ghadimi ,&nbsp;Sophia Blömer ,&nbsp;Aysel Şahin Kaya ,&nbsp;Sandra Krüger ,&nbsp;Christoph Röcken ,&nbsp;Heiner Schäfer ,&nbsp;Jumpei Uchiyama ,&nbsp;Shigenobu Matsuzaki ,&nbsp;Wilhelm Bockelmann","doi":"10.1016/j.yexmp.2025.105021","DOIUrl":"10.1016/j.yexmp.2025.105021","url":null,"abstract":"<div><div>Diet and nutrition affect almost every biological process, including multiple chronic diseases, diabetes, and some cancers. However, there are still significant gaps in our understanding of the importance of nutrition and healthy diets in syntrophy with respect to cross-feeding of the microbe-microbe and the microbe-host in the pathobiology of the infectious-inflamed intestinal milieu caused by anaerobic opportunistic bacteria such as <em>Fusobacterium nucleatum</em> (<em>F. nucleatum</em>). We examined the immune outcomes of three-member folate syntrophy and cross-feeding between <em>F. nucleatum</em> bacteria, endogenous folate-producing gut bacteria, and host cells at the host-pathogen interface using a triple co-culture model. T84, THP-1, and Huh7 cells were inoculated with <em>F. nucleatum</em> for 6 h in regular DMEM, DMEM with 9.5 μM folic acid, or with/without a mixture of <em>Bifidobacterium longum</em> subsp. <em>infantis</em> (<em>B. infantis</em>) and <em>Escherichia coli</em> Nissle <em>1917</em> (EcN). Cytokine secretion, cometabolite levels (ammonia, indoles), cell viability, and barrier integrity were assessed. <em>F. nucleatum-</em>induced folate depletion was associated with increased IL-1β and IL-6 and decreased IL-22, along with reduced transepithelial electrical resistance (TEER) and cell viability in T84 cells. Folate supplementation mitigated these effects. The mixture of <em>B. infantis</em> and EcN reduced <em>F. nucleatum</em>-induced pro-inflammatory cytokines, increased IL-22, and improved TEER and cell viability. These protective effects were enhanced by the addition of folate. <em>F. nucleatum</em> also elevated ammonia and reduced indoles, effects reversed by <em>B. infantis</em> and EcN. In addition to the intrinsic pathogenicity of harmful bacteria, folate deprivation, microbe–microbe folate syntrophy, and microbe–host folate cross-feeding contribute to the pathobiology of anaerobic opportunistic bacteria and influence the physiological fate of host cells. A combination of <em>B. infantis</em> and EcN modulates the infectious-inflamed interface through a cytoprotective effect and mechanical competitive extrusion of pathogenic <em>F. nucleatum</em>. These results provide potential insights into the mechanisms of early-onset colorectal cancer, and evidently, require future studies using patient-derived organoids and in vivo systems to improve clinical relevance.</div></div>","PeriodicalId":12176,"journal":{"name":"Experimental and molecular pathology","volume":"145 ","pages":"Article 105021"},"PeriodicalIF":3.7,"publicationDate":"2026-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145911261","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":"Understanding diabetes and its complications through the lens of Drosophila","authors":"Supriya Bevinakoppamath ,&nbsp;Anju Srinivas ,&nbsp;Chandan Gowda Umesha ,&nbsp;Akila Prashant ,&nbsp;Amanjot Singh ,&nbsp;Vinay Kumar Rao","doi":"10.1016/j.yexmp.2025.105017","DOIUrl":"10.1016/j.yexmp.2025.105017","url":null,"abstract":"<div><div>A significant gap exists between preclinical findings in animal models and their translation to diabetes therapeutics. Although several generic drugs are currently available, an effective and precise control of glycemia is challenging, and side effects due to both hyperglycemia and drugs are common. This is partly due to our incomplete understanding of disease mechanisms. It is now appreciated that, due to its simplicity and well-conserved genetic pathways, Drosophila disease modeling is an excellent choice for studying diabetes and its complications. Here, we review knowledge about conserved glucose sensing mechanisms, energy homeostasis pathways, and diabetes modeling in Drosophila. We discuss how hyperglycemia-induced metabolic deregulations cause diabetic complications. Further through the lens of Drosophila, we highlight molecular mechanisms underlying vascular and emerging diabetic complications, including neurodegeneration and cancer. We conclude with the thought that diabetes modeling in Drosophila could prove beneficial in large-scale screening of drugs for diabetes and its complications.</div></div>","PeriodicalId":12176,"journal":{"name":"Experimental and molecular pathology","volume":"145 ","pages":"Article 105017"},"PeriodicalIF":3.7,"publicationDate":"2025-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145767638","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":"Stereological quantification of tumor infiltrating immune cells as predictor of immunotherapy in metastatic melanoma","authors":"Lenka Vaňková ,&nbsp;Jiří Polívka ,&nbsp;Věra Křížková ,&nbsp;Samuel Vokurka ,&nbsp;Ondřej Fiala ,&nbsp;Monika Holubová ,&nbsp;Kristýna Pivovarčíková ,&nbsp;Inka Třešková ,&nbsp;Tereza Knížková ,&nbsp;Jan Říčař ,&nbsp;Radek Kučera ,&nbsp;Martin Pešta","doi":"10.1016/j.yexmp.2025.105016","DOIUrl":"10.1016/j.yexmp.2025.105016","url":null,"abstract":"<div><div>Immunotherapy by immune checkpoint inhibitors (ICIs) revolutionized the treatment of melanoma patients. Tumor-infiltrating immune cells (TIICs) play a crucial role in antitumor immunity activated by ICIs. However, ICIs treatment may be associated with serious immune-related adverse events (irAEs). The aim of the study was to identify the key immune cells and molecules of the tumor microenvironment responsible for the treatment effects and risk of irAEs through immunohistochemical quantification of TIICs. We analyzed metastases (FFPE) of 28 melanoma patients treated with ICIs. Multilevel sampling and stereological quantification were used to assess TIICs identified immunohistochemically by the markers CD1a, CD1d, CD3, CD4, CD8, CD20, CD56, CD68, FOXP3, including immune checkpoint molecules LAG3, PD1, PD-L1. In lymph node metastases, higher infiltration of PD-L1, CD8-positive cells and lower infiltration of CD1a-positive cells predicted response to ICIs (<em>P</em> ≤ 0.05, P ≤ 0.05, P ≤ 0.05, resp.). In all metastasis's subtypes, higher expression of PD-L1 was predictor of response to immunotherapy (P ≤ 0.05). Lower PD-L1 expression (P ≤ 0.05) and lower CD3 expression (<em>P</em> ≤ 0.001) were associated with irAEs. Higher infiltration of CD8-positive T lymphocytes was associated with longer progression-free survival (<em>P</em> = 0.0166) as well as overall survival (<em>P</em> = 0.0454). Stereological quantification of specific immune cells in melanoma metastases, such as T-lymphocytes (CD3), cytotoxic T-lymphocytes (CD8), dendritic cells (CD1a) and PD-L1-positive cells, may predict ICIs treatment efficacy or the risk of irAEs. High infiltration of metastatic tissue by CD8-positive T cells is important for long-term favorable therapeutic response to ICIs.</div></div>","PeriodicalId":12176,"journal":{"name":"Experimental and molecular pathology","volume":"145 ","pages":"Article 105016"},"PeriodicalIF":3.7,"publicationDate":"2025-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145735408","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":"Seizure susceptibility relates to microglial TREM2 expression and morphology in a multiple repeated low-dose kainic acid model","authors":"Hyo Jung Shin ,&nbsp;In Soo Kim ,&nbsp;Minwoo Kim ,&nbsp;Seung Yeon Jung ,&nbsp;Dong Woon Kim ,&nbsp;Joon Won Kang","doi":"10.1016/j.yexmp.2025.105014","DOIUrl":"10.1016/j.yexmp.2025.105014","url":null,"abstract":"<div><div>Microglia, the resident immune cells of the brain, play a critical role in maintaining homeostasis. In this study, we investigated changes in microglial phenotype associated with seizure susceptibility. Kainic acid (KA) was injected intraperitoneally, and when seizures reached Racine stage 4/5, administration was stopped, and mice were monitored for 60 min. Only mice that showed behavioral convulsive status epilepsy (SE) in the first experiment received a second KA injection 2 weeks later. Using this model, we observed changes in brain tissue and microglial phenotype according to seizure susceptibility. We also analyzed gene expression patterns associated with microglial phagocytosis in a publicly available hippocampal transcriptome microarray dataset (GSE88992) from mice injected with KA. After the initial low-dose KA repeat injection, the number of injections required to induce SE during the secondary injection was compared with the initial injection, and mice were categorized into seizure-resistant (SR, <em>n</em> = 26, no SE), seizure-tolerant (ST, <em>n</em> = 11, SE after ≥2 injections), and seizure-susceptible (SS, <em>n</em> = 15, SE after ≤2 injections) groups. Neuronal loss was observed in all seizure groups, but the extent varied across hippocampal regions. Microglial phenotypes in the hippocampus showed significant differences between groups. Immunofluorescence staining further confirmed that triggering receptor expressed on myeloid cells (TREM2) expression was increased in microglia in the SS group. Using a model that classifies seizure resistance, tolerance, and susceptibility, we observed significant differences in microglial phenotypes and TREM2 expressions between groups. This study highlights the role of microglia in the progression from first seizures to subsequent seizures, a critical step in the development of epilepsy.</div></div>","PeriodicalId":12176,"journal":{"name":"Experimental and molecular pathology","volume":"145 ","pages":"Article 105014"},"PeriodicalIF":3.7,"publicationDate":"2025-12-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145683828","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":"miR-21-5p dysregulation is associated with gut microbiota dysbiosis and pro-oncogenic markers in primary sclerosing cholangitis with concomitant inflammatory bowel disease","authors":"André Anastácio Santos ,&nbsp;David Pires ,&nbsp;Vanda Marques ,&nbsp;Nicole Alesina ,&nbsp;Pedro Miguel Rodrigues ,&nbsp;Ana Catarina Bravo ,&nbsp;Catarina Gouveia ,&nbsp;Susana Saraiva ,&nbsp;Luís Correia ,&nbsp;Ricardo Crespo ,&nbsp;João Pereira da Silva ,&nbsp;Marília Cravo ,&nbsp;Jesus Maria Banales ,&nbsp;Joana Torres ,&nbsp;Cecília Maria Pereira Rodrigues","doi":"10.1016/j.yexmp.2025.105013","DOIUrl":"10.1016/j.yexmp.2025.105013","url":null,"abstract":"<div><h3>Background</h3><div>Primary sclerosing cholangitis (PSC) is a chronic liver disease frequently associated with inflammatory bowel disease (IBD) and increased risk of colorectal cancer (CRC). Despite the strong association, the underlying mechanisms linking PSC-IBD, gut inflammation, and neoplastic potential remain unclear. This study explores the role of miR-21-5p dysregulation, gut microbiota dysbiosis, and pro-oncogenic markers in shaping the inflammatory and neoplastic microenvironment in PSC-IBD patients.</div></div><div><h3>Methods</h3><div>A case-control study was conducted, including PSC patients with concomitant IBD (<em>n</em> = 14) and control individuals without diagnosed PSC and IBD (<em>n</em> = 20). miR-21-5p levels were evaluated in serum, fecal samples, and colonic biopsies <em>via</em> qPCR. Gut microbiota composition was analyzed using 16S rRNA sequencing. Pro-oncogenic and inflammatory markers in colonic tissue were assessed <em>via</em> qPCR. <em>In vitro</em> studies were performed using cholangiocyte (H69), colorectal cancer (HCT116), and primary monocyte models to investigate the role of miR-21-5p.</div></div><div><h3>Results</h3><div>miR-21-5p was significantly upregulated in the right colon, serum, and fecal samples of PSC-IBD patients compared to controls. Gut microbiota analysis revealed dysbiosis, characterized by an increased <em>Bacteroidota</em>/<em>Bacillota</em> ratio and reduction in bile acid-metabolizing bacteria, including <em>Clostridium sensu stricto 1</em>, <em>Ruminococcaceae UCG-002</em>, and <em>Christensenellaceae_R7_group</em>. Colonic tissue analysis showed increased expression of EMT-related transcription factors <em>TWIST1</em> and <em>SNAIL</em>, inflammatory cytokines <em>IL-8</em>, <em>CCL2</em>, and <em>COX2</em>, and the stem cell marker <em>LGR5</em>. <em>In vitro</em> studies confirmed miR-21-5p role in upregulating <em>does</em> markers in monocytes and CRC cells.</div></div><div><h3>Conclusion</h3><div>This study found a link between miR-21-5p dysregulation and gut microbiota dysbiosis, colonic inflammation, and pro-oncogenic signaling in PSC-IBD patients. These findings highlight miR-21-5p as a potential modulator of disease progression and neoplastic risk.</div></div>","PeriodicalId":12176,"journal":{"name":"Experimental and molecular pathology","volume":"145 ","pages":"Article 105013"},"PeriodicalIF":3.7,"publicationDate":"2025-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145683827","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":"Retraction notice to “MICA/B expression in macrophage foam cells infiltrating atherosclerotic plaques” [Experimental and Molecular Pathology 97 (2014) 171–175]","authors":"Shunji Ikeshita,&nbsp;Yukiko Miyatake,&nbsp;Noriyuki Otsuka,&nbsp;Masanori Kasahara","doi":"10.1016/j.yexmp.2025.104981","DOIUrl":"10.1016/j.yexmp.2025.104981","url":null,"abstract":"","PeriodicalId":12176,"journal":{"name":"Experimental and molecular pathology","volume":"144 ","pages":"Article 104981"},"PeriodicalIF":3.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144590773","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}