European Journal of Histochemistry最新文献_第2页

Targeting EphA2 suppresses the proliferation, migration and invasion of endometriosis via the AMPK signaling pathway. 靶向EphA2通过AMPK信号通路抑制子宫内膜异位症的增殖、迁移和侵袭。

IF 2.1 4区生物学

European Journal of Histochemistry Pub Date : 2025-06-17 DOI: 10.4081/ejh.2025.4168

Chaoyi Yang, Shujun Wang, Mengru Li, Xiangli Pang, Aili Tan

引用次数: 0

NR4A3 suppresses bladder cancer progression by modulating autophagy via the PI3K/AKT/mTOR pathway. NR4A3通过PI3K/AKT/mTOR通路调节自噬抑制膀胱癌进展。

IF 2.1 4区生物学

European Journal of Histochemistry Pub Date : 2025-06-17 Epub Date: 2025-06-30 DOI: 10.4081/ejh.2025.4221

Li Fan, Feng Xu, Shouyong Liu, Ding Wu, Suchun Wang, Xin Pan, Yulin Zhou, Le Qu, Wenquan Zhou

{"title":"NR4A3 suppresses bladder cancer progression by modulating autophagy via the PI3K/AKT/mTOR pathway.","authors":"Li Fan, Feng Xu, Shouyong Liu, Ding Wu, Suchun Wang, Xin Pan, Yulin Zhou, Le Qu, Wenquan Zhou","doi":"10.4081/ejh.2025.4221","DOIUrl":"10.4081/ejh.2025.4221","url":null,"abstract":"Bladder cancer (BC) is a prevalent and aggressive malignancy with high recurrence. Autophagy plays a dual role in cancer, acting as a tumor suppressor early on and promoting survival in later stages. NR4A3, a nuclear receptor with tumor-suppressive effects in other cancers, has not been explored in BC. NR4A3 expression was analyzed using TCGA data and validated in clinical BC samples via immunohistochemistry and RT-qPCR. NR4A3-overexpressing BC cell lines (5637, T24) were created using lentiviral vectors. Cell viability, proliferation, migration, and invasion were assessed through CCK-8, EdU, and Transwell assays. Autophagy was measured by microtubule-associated protein 1A/1B-light chain 3 (LC3), autophagy-related protein 5 (ATG5), Beclin-1 and p62 expression via immunofluorescence and Western blotting. The phosphoinositide 3-kinase (PI3K) / protein kinase B (AKT) / mammalian target of rapamycin (mTOR) pathway was examined by assessing phosphorylation levels. It was found that NR4A3 was significantly downregulated in BC tissues. Overexpression of NR4A3 inhibited BC cell proliferation, migration, and invasion, while promoting apoptosis. NR4A3 overexpression increased autophagy markers and suppressed PI3K/AKT/mTOR signaling. Autophagy inhibition reversed these effects. In conclusion, NR4A3 suppresses BC progression by promoting autophagy via the PI3K/AKT/mTOR pathway. Targeting NR4A3-mediated autophagy may provide a novel therapeutic strategy for BC.","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"69 3","pages":""},"PeriodicalIF":2.1,"publicationDate":"2025-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12264721/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144530892","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

circRNA-79530 regulates Twist-mediated mitochondrial damage via sponging miR-214 affecting hypoxia/reoxygenation-induced injury in H9c2 cardiomyocytes. circRNA-79530通过海绵miR-214调控twist介导的线粒体损伤，影响缺氧/再氧化诱导的H9c2心肌细胞损伤。

IF 2.1 4区生物学

European Journal of Histochemistry Pub Date : 2025-06-17 Epub Date: 2025-08-22 DOI: 10.4081/ejh.2025.4230

Ziyang Yu, Wenbo Xu, Yirong Teng, Tingting Li, Ren Guo, Ju Li, Xichen Li, Yanping Li, Yinglu Hao

{"title":"circRNA-79530 regulates Twist-mediated mitochondrial damage via sponging miR-214 affecting hypoxia/reoxygenation-induced injury in H9c2 cardiomyocytes.","authors":"Ziyang Yu, Wenbo Xu, Yirong Teng, Tingting Li, Ren Guo, Ju Li, Xichen Li, Yanping Li, Yinglu Hao","doi":"10.4081/ejh.2025.4230","DOIUrl":"10.4081/ejh.2025.4230","url":null,"abstract":"Cardiomyocyte injury related to hypoxia/reoxygenation (H/R) is pivotal in myocardial infarction. The circular RNA circRNA-79530 (circ79530) may play a regulatory role in this process, though its exact function has yet to be elucidated. This research explores the role of circRNA-79530 in H9c2 cells under H/R, with a particular focus on its interactions with miR-214 and the transcription factor Twist. It also examines their subsequent effects on mitochondrial function and oxidative stress. H9c2 cardiomyocytes were subjected to H/R to model myocardial injury. We measured circRNA-79530, miR-214, and Twist levels via RT-qPCR, with Twist protein via Western blotting. ROS levels were quantified using DCFH-DA, and cell viability and injuries were assessed through CCK-8, LDH, SOD, and MDA assays, respectively. Mitochondrial performance was assessed through various methods, including the measurement of mitochondrial membrane potential using JC-1 staining, the quantification of ATP levels, and the examination of the protein levels of mitochondrial complexes, as well as the expression of fusion proteins. Our findings indicated that downregulation of circRNA-79530 modulated miR-214 and Twist expression, influencing mitochondrial dynamics and ROS production. Knockdown of circRNA-79530 improved cell viability, reduced oxidative stress and enhanced mitochondrial function. Additionally, overexpression of miR-214 mitigated Twist expression, further supporting the effect of miR-214 in H/R conditions. circRNA-79530 could worsen oxidative stress and mitochondrial dysfunction, and regulate Twist-mediated mitochondrial damage via sponging miR-214 in H9c2 cells under H/R conditions.","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"69 3","pages":""},"PeriodicalIF":2.1,"publicationDate":"2025-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12421722/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144977246","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Effects of Notch signaling on proliferation, angiogenesis, and adipogenesis of hemangioma-derived stem cells. Notch信号对血管瘤干细胞增殖、血管生成和脂肪生成的影响。

IF 2.1 4区生物学

European Journal of Histochemistry Pub Date : 2025-06-17 Epub Date: 2025-09-01 DOI: 10.4081/ejh.2025.4241

Weidong Wang, Sheng Chen, Yuan Wang, Cui Jie, Weimin Shen

{"title":"Effects of Notch signaling on proliferation, angiogenesis, and adipogenesis of hemangioma-derived stem cells.","authors":"Weidong Wang, Sheng Chen, Yuan Wang, Cui Jie, Weimin Shen","doi":"10.4081/ejh.2025.4241","DOIUrl":"10.4081/ejh.2025.4241","url":null,"abstract":"Hemangioma-derived stem cells (Hem-SCs) constitute the cellular basis for adipogenesis during infantile hemangioma (IH) regression, with Notch signaling implicated in this process. To elucidate Notch's role in Hem-SCs biology, we isolated primary Hem-SCs from proliferative-phase IH specimens and validated their stem cell characteristics. Three days post-intervention with the γ-secretase inhibitor DAPT (N‑[N‑(3,5‑difluorophenacetyl)‑L‑alanyl]‑S‑phenylglycine t‑butylester), we assessed Notch and PI3K/AKT signaling dynamics while concurrently measuring vascular endothelial growth factor receptor (VEGFR) protein expression. Cellular proliferation was quantified via CCK-8 assay. During adipogenic differentiation (Day 14), RTqPCR evaluated Notch pathway genes (Notch1, Jagged1, Hes1), while adipogenic commitment was determined through Oil Red O staining and adipocyte-specific gene expression (PPARγ, C/EBPα). We demonstrate that DAPT suppresses Notch and PI3K/AKT signaling in Hem-SCs, concomitantly enhancing cellular proliferation and angiogenesis. Simultaneous analysis of VEGFR expression revealed differential DAPT-mediated regulation: VEGFR1 downregulation with concomitant VEGFR2 upregulation. During adipogenic induction, Notch pathway genes (Notch1, Jagged1, Hes1) were significantly downregulated. DAPT treatment further elevated adipogenic markers (PPARγ, C/EBPα) and lipid accumulation. Crucially, co-administration of the PI3K activator 740Y-P reversed DAPT-induced adipogenesis. Mechanistically, Notch inhibition promotes Hem-SCs proliferation, angiogenesis, and adipocyte differentiation by attenuating PI3K/AKT signaling.","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"69 3","pages":""},"PeriodicalIF":2.1,"publicationDate":"2025-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12439523/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144977338","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Forever particles: histochemistry in the plasticene age. 永久粒子：塑粒时代的组织化学。

IF 2.1 4区生物学

European Journal of Histochemistry Pub Date : 2025-06-17 Epub Date: 2025-08-01 DOI: 10.4081/ejh.2025.4226

Beatrice Camia, Andrea Casasco, Manuela Monti

{"title":"Forever particles: histochemistry in the plasticene age.","authors":"Beatrice Camia, Andrea Casasco, Manuela Monti","doi":"10.4081/ejh.2025.4226","DOIUrl":"10.4081/ejh.2025.4226","url":null,"abstract":"The statement \"Plastics define the way we live today\" summarizes the findings of the Plastic Europe 2020 final document (https://plasticseurope.org/knowledge-hub/plastics-the-facts-2020/). Sadly, this also means that the plastic waste generated over the next decade is likely to become unmanageable. By 2050, plastic usage is expected to triple, resulting in a similar increase in plastic waste, with approximately half of it ending up in landfills. Emerging research indicates that micro and nanoplastics have been found in various human organs, including the gonads, placenta, blood, arteries, lungs, liver, kidney, and even the brain. This raises significant questions about their pervasive presence within our bodies and their potential threat to health. In addition to their harmful effects, these \"forever particles\" (micro/nanoplastics) can serve as Trojan horses, transporting additional pollutants such as bacteria and heavy metals into our bodies. In this review, we explore key aspects of the plastics crisis and urge the scientific community -especially those in the fields of cytochemistry and histochemistry, which adeptly connect morphology with function- to investigate the harmful effects of micro and nanoplastics that we encounter daily through ingestion or inhalation. This research should focus on various physiological levels, including DNA, cells, and tissues.","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"69 3","pages":""},"PeriodicalIF":2.1,"publicationDate":"2025-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12406116/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144977292","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Solamargine inhibited the progression of non-small cell lung cancer in vitro by activating T cells. Solamargine通过激活T细胞抑制体外非小细胞肺癌的进展。

IF 2.1 4区生物学

European Journal of Histochemistry Pub Date : 2025-06-17 Epub Date: 2025-09-01 DOI: 10.4081/ejh.2025.4217

Changchun Zhang, Yichen Sun, Wei Jiang, Lin Wu, Qi Fang, Qikun Wang

{"title":"Solamargine inhibited the progression of non-small cell lung cancer in vitro by activating T cells.","authors":"Changchun Zhang, Yichen Sun, Wei Jiang, Lin Wu, Qi Fang, Qikun Wang","doi":"10.4081/ejh.2025.4217","DOIUrl":"10.4081/ejh.2025.4217","url":null,"abstract":"Lung cancer is the leading cause of cancer-related death globally and the most common cancer type. Solamargine is an extract from the traditional Chinese medicine, Long Kui, which exhibits antitumor effects in a number of cancer types, including lung cancer. However, the possible association between solamargine and the tumor microenvironment (TME) in non-small cell lung cancer (NSCLC) remains to be elucidated. In the present study, Cell Counting Kit-8 and 5-Ethynyl-2'-deoxyuridine (EdU) assays were used to evaluate the viability and proliferation of NSCLC cells, respectively. In addition, NSCLC cells were co-cultured with peripheral blood mononuclear cells with or without prior solamargine treatment to evaluate the possible association between solamargine and the TME. The results indicated that solamargine can inhibit NSCLC cell proliferation and migration directly. In addition, it was demonstrated that solamargine can prevent the progression of NSCLC indirectly via activating the function of T cells. These findings may provide a novel theoretical basis in drug discovery for the treatment of NSCLC.","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"69 3","pages":""},"PeriodicalIF":2.1,"publicationDate":"2025-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12439524/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144977288","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Aloe-emodin ameliorates chronic kidney disease fibrosis by inhibiting PI3K-mediated signaling pathway. 芦荟大黄素通过抑制pi3k介导的信号通路改善慢性肾脏疾病纤维化。

IF 2.1 4区生物学

European Journal of Histochemistry Pub Date : 2025-06-17 Epub Date: 2025-08-06 DOI: 10.4081/ejh.2025.4228

Ming Chen, Wenhui Zhu, Yao Chen, Jingying Shang, Wenfan Wang, Xiaoming Yan, Peng Liu, Yabin Zhou

{"title":"Aloe-emodin ameliorates chronic kidney disease fibrosis by inhibiting PI3K-mediated signaling pathway.","authors":"Ming Chen, Wenhui Zhu, Yao Chen, Jingying Shang, Wenfan Wang, Xiaoming Yan, Peng Liu, Yabin Zhou","doi":"10.4081/ejh.2025.4228","DOIUrl":"10.4081/ejh.2025.4228","url":null,"abstract":"Chronic kidney disease (CKD) impacts a vast number of individuals worldwide, culminating in renal fibrosis. Renal fibrosis serves as the main reason for end-stage renal failure. However, the current targeted treatment methods for renal fibrosis remain scarce. Aloe-emodin (AE) is a naturally occurring compound discovered in rhubarb and aloe. In this research, we investigated the underlying mechanisms of AE in adenine-induced mouse renal fibrosis models and TGFβ-1 stimulated renal tubular epithelial cells (HK-2). It was discovered that AE not only decelerated the decline of renal function in adenine-treated mice but also suppressed the expression of Collagen I and Fibronectin. Furthermore, network pharmacology analysis suggested that AE's treatment of renal fibrosis might function via the PI3K/Akt/GSK3β signaling pathway. In vivo and in vitro Western blot and immunofluorescence findings demonstrate that AE significantly resists the advancement of renal fibrosis by inhibiting α-smooth muscle actin (α-SMA) and vimentin. Simultaneously, findings from 740Y-P (a PI3K agonist) and siRNA (PI3K) indicate that AE inhibits the expression of the PI3K/Akt/GSK3β cascade by lowering PI3K's phosphorylation level. From a mechanistic perspective, through molecular docking and plasmid transfection, the specific base sequence of PI3K in HK-2 cells was altered for experimental validation. The outcomes illustrate that AE can directly bind with PI3K, inhibiting its activation, impeding the PI3K/Akt/GSK3β signal transmission, thereby ultimately suppressing renal fibrosis progression. In conclusion, PI3K/Akt/GSK3β is a potential therapeutic target for CKD-related renal fibrosis, making AE a promising new treatment alternative for this condition.","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"69 3","pages":""},"PeriodicalIF":2.1,"publicationDate":"2025-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12406115/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144977166","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Proceedings of the 70th Congress of the Italian Embryological Group-Italian Society of Development and Cell Biology (GEI-SIBSC). 意大利胚胎学组-意大利发育与细胞生物学学会（GEI-SIBSC）第70届大会论文集。

IF 2.1 4区生物学

European Journal of Histochemistry Pub Date : 2025-06-09 DOI: 10.4081/ejh.2025.4245

The Scientific Committee

引用次数: 0

Cancer cell-derived exosomal miR-34a inhibits the malignant progression of pancreatic adenocarcinoma cells by restraining the M2 polarization of macrophages. 癌细胞来源的外泌体miR-34a通过抑制巨噬细胞的M2极化抑制胰腺腺癌细胞的恶性进展。

IF 2.1 4区生物学

European Journal of Histochemistry Pub Date : 2025-04-07 Epub Date: 2025-04-17 DOI: 10.4081/ejh.2025.4176

Kui Long, Xiang Kui, Qingbin Zeng, Wenzhi Dong

{"title":"Cancer cell-derived exosomal miR-34a inhibits the malignant progression of pancreatic adenocarcinoma cells by restraining the M2 polarization of macrophages.","authors":"Kui Long, Xiang Kui, Qingbin Zeng, Wenzhi Dong","doi":"10.4081/ejh.2025.4176","DOIUrl":"https://doi.org/10.4081/ejh.2025.4176","url":null,"abstract":"This study aimed to investigate the crosstalk mechanism between pancreatic cancer (PAC) cells and M2 tumor-associated macrophages induced by tumor-derived exosomal miR-34a. MicroRNA and mRNA expression levels were detected using RT-qPCR. Cell Counting Kit-8, wound-healing, transwell assays and flow cytometry were respectively employed to assess cell proliferation, migration, invasion and apoptosis. Enzyme-linked immunosorbent assay was utilized to determine cytokine secretion. Transmission electron microscopy and nanoparticle tracking analyses were performed to detect the exosome morphology and particle size. Phagocytosis of exosomes by macrophages was verified by PKH26 labeling. The effects of exosome-treated macrophages on the epithelial-mesenchymal transition, invasion, and migration of PANC-1 cells were investigated using coculture experiments. The identification of miR-34a's potential targets were determined with TargetScan and validated by a dual-luciferase reporter assay. miR-34a was expressed at low levels in PAC tissues, cells, and exosomes. The overexpression of miR-34a restrains the malignant progression of PANC-1 cells. After miR-34a-overexpressed PANC-1-derived exosomes were phagocytosed by macrophages, the process of M2 polarization in macrophages was obstructed, leading to the suppression of epithelial-mesenchymal transition, migration, and invasion of the cocultured PANC-1 cells. Suppressor of cytokine signaling 3 is a direct target of miR-34a. MiR-34a negatively modulates the suppressor of cytokine signaling 3 to prevent the M2 polarization of macrophages by engaging the Janus kinase/signal transducers and activators of the transcription pathway and influencing the malignancy of PAC cells. miR-34a in cancer cell-derived exosomes inhibits the malignant progression of pancreatic cancer cells by restraining M2 polarization of macrophages.","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"69 2","pages":""},"PeriodicalIF":2.1,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12051414/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144056556","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Downregulation of S100 calcium-binding A4 (S100A4) ameliorates hepatic fibrosis via regulating Wnt/β-catenin signaling pathway. 下调S100钙结合A4 （S100A4）通过调节Wnt/β-catenin信号通路改善肝纤维化。

IF 2.1 4区生物学

European Journal of Histochemistry Pub Date : 2025-04-07 Epub Date: 2025-04-14 DOI: 10.4081/ejh.2025.4186

Chixian Zhang, Kai Bai, Dexu Li

{"title":"Downregulation of S100 calcium-binding A4 (S100A4) ameliorates hepatic fibrosis via regulating Wnt/β-catenin signaling pathway.","authors":"Chixian Zhang, Kai Bai, Dexu Li","doi":"10.4081/ejh.2025.4186","DOIUrl":"https://doi.org/10.4081/ejh.2025.4186","url":null,"abstract":"S100 calcium-binding protein A4 (S100A4), a fibrosis-associated calcium-binding protein, has been implicated in fibrotic progression across multiple organs. Activation of the Wnt/β-catenin signaling pathway is a critical driver of hepatic fibrosis, yet the mechanistic role of S100A4 in this context remains poorly defined. This study investigated the regulatory role of S100A4 in hepatic fibrosis in vitro and in vivo. Hepatic stellate cells (HSCs) were treated with TGF-β to induce fibrotic activation, and S100A4 expression was silenced using shRNA. A carbon tetrachloride (CCl₄)-induced murine hepatic fibrosis model was employed for in vivo validation. Fibrotic markers, including collagen I, fibronectin, and α-smooth muscle actin (α-SMA), were assessed via qRT-PCR, Western blotting, immunofluorescence, and immunohistochemistry. Liver histopathology and function were evaluated using Masson trichrome staining, hematoxylin-eosin staining, and serum ALT/AST assays. In vitro experiments demonstrated that TGF-β treatment upregulated S100A4 expression in HSCs, while S100A4 silencing suppressed HSC activation, extracellular matrix (ECM) deposition, and Wnt/β-catenin signaling. In vivo, S100A4 downregulation attenuated CCl₄-induced hepatic fibrosis, reduced collagen accumulation, improved liver histology, and normalized serum ALT/AST levels. These findings indicate that S100A4 promotes hepatic fibrosis by activating the Wnt/β-catenin pathway, highlighting its potential as a therapeutic target.","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"69 2","pages":""},"PeriodicalIF":2.1,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12051413/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144042104","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0