Journal of Cellular Physiology最新文献_第3页

Pharmacological activity, phytochemistry, and organ protection of lithospermic acid. 石杉碱甲的药理活性、植物化学和器官保护。

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2024-10-14 DOI: 10.1002/jcp.31460

Wenwen Yang, Jiayan Li, Jiayin Tian, Xiaoyi Liu, Wentao Xie, Xue Wu, Zhe Zhang, Yuefei Song, Shuya Wang, Shiyan Zhao, Zheng Wang, Yang Yang, Zhenxiao Jin

{"title":"Pharmacological activity, phytochemistry, and organ protection of lithospermic acid.","authors":"Wenwen Yang, Jiayan Li, Jiayin Tian, Xiaoyi Liu, Wentao Xie, Xue Wu, Zhe Zhang, Yuefei Song, Shuya Wang, Shiyan Zhao, Zheng Wang, Yang Yang, Zhenxiao Jin","doi":"10.1002/jcp.31460","DOIUrl":"https://doi.org/10.1002/jcp.31460","url":null,"abstract":"Lithospermic acid (LA) is a water-soluble phenolic acid compound extracted and separated from the dried root and the rhizome of Salviamiltiorrhiza Bge (Labiatae), possessing multiple biological activities. Firstly, in terms of pharmacological activities, LA has been proven to possess anti-inflammatory, antioxidant, autophagy activation, and antiapoptotic properties. Secondly, the pharmacokinetic characteristics of LA show rapid and extensive distribution in various tissues after intravenous administration, followed by rapid elimination and excretion. Additionally, potential therapeutic effects of LA have been found in various diseases such as thrombosis, Parkinson's disease, hepatitis B, diabetes, and psoriasis, among others. Particularly, LA has shown promising prospects in the treatment of clinical heart diseases and has been included in new drug formulations for the treatment of chronic angina, demonstrating superior efficacy compared to current cardiovascular drugs. In conclusion, this review comprehensively introduces the pharmacological mechanisms, pharmacokinetics, and protective effects in diseases of LA. These information can lay a theoretical foundation for the future development and new clinical applications of LA.","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":" ","pages":"e31460"},"PeriodicalIF":4.5,"publicationDate":"2024-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142466379","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Leukotriene B4 is elevated in diabetes and promotes ventricular arrhythmogenesis in guinea pig. 白三烯 B4 在糖尿病患者体内升高，并促进豚鼠室性心律失常的发生。

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2024-10-14 DOI: 10.1002/jcp.31467

Andrea Corbin, Kelly A Aromolaran, Ademuyiwa S Aromolaran

{"title":"Leukotriene B4 is elevated in diabetes and promotes ventricular arrhythmogenesis in guinea pig.","authors":"Andrea Corbin, Kelly A Aromolaran, Ademuyiwa S Aromolaran","doi":"10.1002/jcp.31467","DOIUrl":"https://doi.org/10.1002/jcp.31467","url":null,"abstract":"Diabetes (DM) patients have an increased risk (~50%) for sudden cardiac death (SCD), mostly as a result of ventricular arrhythmias. The molecular mechanisms involved remain partially defined. The potent proinflammatory lipid mediator leukotriene (LT) B4, is pathologically elevated in DM compared to nondiabetic patients, resulting in increased LTB4 accumulation in heart, leading to an increased risk for life-threatening proarrhythmic signatures. We used electrophysiology, immunofluorescence, and confocal microscopy approaches to evaluate LTB4 cellular effects in guinea pig heart and ventricular myocytes. We have observed that LTB4 is increased in multiple mouse models (C57BL/6 J/Lepob/ob and PANIC-ATTAC) of DM, promotes profound cellular arrhythmogenesis (spontaneous beats and early after depolarizations, EADs), and severely depresses the rapidly activating delayed rectifier K current (hERG1/IKr) density in HEK293 cells and guinea pig ventricular myocytes. We have further found that guinea pigs challenged with LTB4 displayed a significantly prolonged QT interval, and that this can be prevented with LTB4R inhibition, suggesting that preventing such LTB4R effects may be therapeutically beneficial in DM. Our data suggests that a further elucidation of LTB4 vulnerable substrates, and how this leads to ventricular arrhythmias, is likely to lead to continued improvements in management options, and the development of new therapies for prevention of SCD in DM patients.","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":" ","pages":"e31467"},"PeriodicalIF":4.5,"publicationDate":"2024-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142466378","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Corrigendum: RA promotes proliferation of primordial germ cell-like cells differentiated from porcine skin-derived stem cells. 更正：RA可促进由猪皮肤干细胞分化而来的原始生殖细胞样细胞的增殖。

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2024-10-14 DOI: 10.1002/jcp.31470

引用次数: 0

Advances in the mechanisms of vascular calcification in chronic kidney disease. 慢性肾脏病血管钙化机制的研究进展。

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2024-10-11 DOI: 10.1002/jcp.31464

Ziyang Wang, Zebin Gui, Lirong Zhang, Zhongqun Wang

{"title":"Advances in the mechanisms of vascular calcification in chronic kidney disease.","authors":"Ziyang Wang, Zebin Gui, Lirong Zhang, Zhongqun Wang","doi":"10.1002/jcp.31464","DOIUrl":"https://doi.org/10.1002/jcp.31464","url":null,"abstract":"Vascular calcification (VC) is common in patients with advanced chronic kidney disease (CKD).A series of factors, such as calcium and phosphorus metabolism disorders, uremic toxin accumulation, inflammation and oxidative stress and cellular senescence, cause osteoblast-like differentiation of vascular smooth muscle cells, secretion of extracellular vesicles, and imbalance of calcium regulatory factors, which together promote the development of VC in CKD. Recent advances in epigenetics have provided better tools for the investigation of VC etiology and new approaches for finding more accurate biomarkers. These advances have not only deepened our understanding of the pathophysiological mechanisms of VC in CKD, but also provided valuable clues for the optimization of clinical predictors and the exploration of potential therapeutic targets. The aim of this article is to provide a comprehensive overview of the pathogenesis of CKD VC, especially the new advances made in recent years, including the various key factors mentioned above. Through the comprehensive analysis, we expect to provide a solid theoretical foundation and research direction for future studies targeting the specific mechanisms of CKD VC, the establishment of clinical predictive indicators and the development of potential therapeutic strategies.","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":" ","pages":"e31464"},"PeriodicalIF":4.5,"publicationDate":"2024-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142400414","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

N-terminomics profiling of naïve and inflamed murine colon reveals proteolytic signatures of legumain. 新生和发炎小鼠结肠的 N 端组学分析揭示了豆豆蛋白酶的蛋白水解特征。

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2024-10-11 DOI: 10.1002/jcp.31466

Alexander R Ziegler, Bethany M Anderson, Rocco Latorre, Rachel M McQuade, Antoine Dufour, Brian L Schmidt, Nigel W Bunnett, Nichollas E Scott, Laura E Edgington-Mitchell

{"title":"N-terminomics profiling of naïve and inflamed murine colon reveals proteolytic signatures of legumain.","authors":"Alexander R Ziegler, Bethany M Anderson, Rocco Latorre, Rachel M McQuade, Antoine Dufour, Brian L Schmidt, Nigel W Bunnett, Nichollas E Scott, Laura E Edgington-Mitchell","doi":"10.1002/jcp.31466","DOIUrl":"10.1002/jcp.31466","url":null,"abstract":"Legumain is a cysteine protease broadly associated with inflammation. It has been reported to cleave and activate protease-activated receptor 2 to provoke pain associated with oral cancer. Outside of gastric and colon cancer, little has been reported on the roles of legumain within the gastrointestinal tract. Using a legumain-selective activity-based probe, LE28, we report that legumain is activated within colonocytes and macrophages of the murine colon, and that it is upregulated in models of acute experimental colitis. We demonstrated that loss of legumain activity in colonocytes, either through pharmacological inhibition or gene deletion, had no impact on epithelial permeability in vitro. Moreover, legumain inhibition or deletion had no obvious impacts on symptoms or histological features associated with dextran sulfate sodium-induced colitis, suggesting its proteolytic activity is dispensable for colitis initiation. To gain insight into potential functions of legumain within the colon, we performed field asymmetric waveform ion mobility spectrometry-facilitated quantitative proteomics and N-terminomics analyses on naïve and inflamed colon tissue from wild-type and legumain-deficient mice. We identified 16 altered cleavage sites with an asparaginyl endopeptidase signature that may be direct substrates of legumain and a further 16 cleavage sites that may be indirectly mediated by legumain. We also analyzed changes in protein abundance and proteolytic events broadly associated with colitis in the gut, which permitted comparison to recent analyses on mucosal biopsies from patients with inflammatory bowel disease. Collectively, these results shed light on potential functions of legumain and highlight its potential roles in the transition from inflammation to colorectal cancer.","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":" ","pages":"e31466"},"PeriodicalIF":4.5,"publicationDate":"2024-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142400415","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

A combination of major histocompatibility complex (MHC) I overexpression and type I interferon induce mitochondrial dysfunction in human skeletal myoblasts. 主要组织相容性复合体（MHC）Ⅰ过表达和Ⅰ型干扰素共同诱导人类骨骼肌母细胞线粒体功能障碍。

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2024-10-09 DOI: 10.1002/jcp.31458

Anastasia Thoma, Razan Alomosh, Holly L Bond, Tania Akter-Miah, Nasser Al-Shanti, Hans Degens, Vanja Pekovic-Vaughan, Adam P Lightfoot

{"title":"A combination of major histocompatibility complex (MHC) I overexpression and type I interferon induce mitochondrial dysfunction in human skeletal myoblasts.","authors":"Anastasia Thoma, Razan Alomosh, Holly L Bond, Tania Akter-Miah, Nasser Al-Shanti, Hans Degens, Vanja Pekovic-Vaughan, Adam P Lightfoot","doi":"10.1002/jcp.31458","DOIUrl":"https://doi.org/10.1002/jcp.31458","url":null,"abstract":"The overexpression of major histocompatibility complex (MHC) I on the surface of muscle fibers is a characteristic hallmark of the idiopathic inflammatory myopathies (IIMs), collectively termed myositis. Alongside MHC-I overexpression, subtypes of myositis, display a distinct type I interferon (IFN) signature. This study examined the combinational effects of elevated MHC-I and type I IFNs (IFNα/β) on mitochondrial function, as mitochondrial dysfunction is often seen in IIMs. Human skeletal muscle myoblasts were transfected with an MHC-I isoform using the mammalian HLA-A2/Kb vector. Mitochondrial respiration, mitochondrial membrane potential, and reactive oxygen/nitrogen species generation were assessed with or without IFNα and IFNβ. We show that MHC-I overexpression in human skeletal muscle myoblasts led to decreased basal glycolysis and mitochondrial respiration, cellular spare respiratory capacity, adenosine triphosphate-linked respiration, and an increased proton leak, which were all exaggerated by type I IFNs. Mitochondrial membrane depolarization was induced by MHC-I overexpression both in absence and presence of type I IFNs. Human myoblasts overexpressing MHC-I showed elevated nitric oxide generation that was abolished when combined with IFN. MHC-I on its own did not result in an increased reactive oxygen species (ROS) production, but IFN on their own, or combined with MHC-I overexpression did induce elevated ROS generation. Surprisingly, we observed no gross changes in mitochondrial reticular structure or markers of mitochondrial dynamics. We present new evidence that MHC-I overexpression and type I IFNs aggravate the effects each has on mitochondrial function in human skeletal muscle cells, providing novel insights into their mechanisms of action and suggesting important implications in the further study of myositis pathogenesis.","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":" ","pages":"e31458"},"PeriodicalIF":4.5,"publicationDate":"2024-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142390769","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Investigation into the significant role of dermal-epidermal interactions in skin ageing utilising a bioengineered skin construct. 利用一种生物工程皮肤结构，研究真皮-表皮相互作用在皮肤老化中的重要作用。

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2024-10-08 DOI: 10.1002/jcp.31463

Lydia Costello, Kirsty Goncalves, Paola De Los Santos Gomez, Ben Hulette, Teresa Dicolandrea, Michael J Flagler, Robert Isfort, John Oblong, Charlie Bascom, Stefan Przyborski

{"title":"Investigation into the significant role of dermal-epidermal interactions in skin ageing utilising a bioengineered skin construct.","authors":"Lydia Costello, Kirsty Goncalves, Paola De Los Santos Gomez, Ben Hulette, Teresa Dicolandrea, Michael J Flagler, Robert Isfort, John Oblong, Charlie Bascom, Stefan Przyborski","doi":"10.1002/jcp.31463","DOIUrl":"https://doi.org/10.1002/jcp.31463","url":null,"abstract":"Increased prevalence of skin ageing is a growing concern due to an ageing global population and has both sociological and psychological implications. The use of more clinically predictive in vitro methods for dermatological research is becoming commonplace due to initiatives and the cost of clinical testing. In this study, we utilise a well-defined and characterised bioengineered skin construct as a tool to investigate the cellular and molecular dynamics involved in skin ageing from a dermal perspective. Through incorporation of ageing fibroblasts into the dermal compartment we demonstrate the significant impact of dermal-epidermal crosstalk on the overlying epidermal epithelium. We characterise the paracrine nature of dermal-epidermal communication and the impact this has during skin ageing. Soluble factors, such as inflammatory cytokines released as a consequence of senescence associated secretory phenotype (SASP) from ageing fibroblasts, are known to play a pivotal role in skin ageing. Here, we demonstrate their effect on epidermal morphology and thickness, but not keratinocyte differentiation or tissue structure. Through a novel in vitro strategy utilising bioengineered tissue constructs, this study offers a unique reductionist approach to study epidermal and dermal compartments in isolation and tandem.","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":" ","pages":"e31463"},"PeriodicalIF":4.5,"publicationDate":"2024-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142390770","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Taurine reduces glycolysis of pig skeletal muscle by inhibiting HIF-1α signaling. 牛磺酸通过抑制 HIF-1α 信号传导减少猪骨骼肌的糖酵解。

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2024-10-07 DOI: 10.1002/jcp.31461

Xiaoling Chen, An Wenting, Huang Zhiqing, Gang Jia, Hua Zhao

{"title":"Taurine reduces glycolysis of pig skeletal muscle by inhibiting HIF-1α signaling.","authors":"Xiaoling Chen, An Wenting, Huang Zhiqing, Gang Jia, Hua Zhao","doi":"10.1002/jcp.31461","DOIUrl":"https://doi.org/10.1002/jcp.31461","url":null,"abstract":"The aim of this study was to investigate the effect of taurine on skeletal muscle glycolysis in pigs. The results showed that dietary supplementation of taurine significantly reduced the activities of hexokinase (HK), phosphofructose kinase (PFK), and pyruvate kinase (PK) in finishing pigs. Meanwhile, taurine reduced the protein and mRNA expression levels of hypoxia inducible factor 1α (HIF-1α) and the mRNA expression of glycolytic enzyme related genes (such as HK type II, HK Ⅱ; pyruvate kinase M2, PKM2; lactate dehydrogenase A, LDHA). In addition, taurine reduced the expression of HIF-1α, lactate content, and the expression of glycolysis related genes in porcine myotubes. These results suggest that taurine may regulate glycolysis in skeletal muscle of finishing pigs through the HIF-1α signaling pathway. To further investigate the mechanism by which taurine affects skeletal glycolysis, HIF-1α activator dimethyloxalyl glycine (DMOG) was used to treat porcine myotubes, our results showed that DMOG significantly increased the protein and mRNA expression levels of HIF-1α, lactate content, and glycolytic enzyme (HK, PFK, PK, and LDH) activity, but taurine treatment significantly inhibited this effect. Taken together, these results of in vivo and in vitro experiments revealed that taurine reduces skeletal muscle glycolysis by inhibiting HIF-1α signaling.","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":" ","pages":"e31461"},"PeriodicalIF":4.5,"publicationDate":"2024-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142380943","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

RETRACTION: Development of an Experimental Animal Model for Lower Back Pain by Percutaneous Injury-Induced Lumbar Facet Joint Osteoarthritis. 回放：通过经皮损伤诱发腰椎面关节骨关节炎，建立下背部疼痛的实验动物模型。

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2024-10-07 DOI: 10.1002/jcp.31455

{"title":"RETRACTION: Development of an Experimental Animal Model for Lower Back Pain by Percutaneous Injury-Induced Lumbar Facet Joint Osteoarthritis.","authors":"","doi":"10.1002/jcp.31455","DOIUrl":"https://doi.org/10.1002/jcp.31455","url":null,"abstract":"Retraction: J.-S. Kim, K. Ahmadinia, X. Li, J. L. Hamilton, S. Andrews, C. A. Haralampus, G. Xiao, H.-M. Sohn, J.-W. You, Y.-S. Seo, G. S. Stein, A. J. Van Wijnen, S.-G. Kim, and H.-J. Im, \"Development of an Experimental Animal Model for Lower Back Pain by Percutaneous Injury-Induced Lumbar Facet Joint Osteoarthritis,\" Journal of Cellular Physiology 230, no. 11 (2015): 2837-2847, https://doi.org/10.1002/jcp.25015. The above article, published online on 9 April 2015 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Robert Heath; and Wiley Periodicals LLC. The retraction has occurred due to concerns related to the data presented in the article raised by the Office of Research Compliance at Rush University Medical Center following an investigation jointly conducted by Rush University and the Jesse Brown Veterans Affairs Medical Center (JBVAMC). Specifically, the journal has been made aware of discrepancies in the reported sample sizes for each of the three experimental groups in Figure 4A, with the indicated numbers exceeding the actual sample sizes. Additionally, image elements of the experimental data in Figure 7A and B were found to have been used by the same author(s) for publication elsewhere in a different scientific context. The corresponding author, Dr. Hee-Jeong Im Sampen, has been informed of the decision to retract but did not agree with it, as she is confident that any errors in the publication do not impact the reliability of the paper's findings. She also advised the editors that she stands ready to cooperate fully to make any necessary corrections. However, the article is retracted as the editors lost trust in the accuracy of the data and consider the conclusions invalid.","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":" ","pages":"e31455"},"PeriodicalIF":4.5,"publicationDate":"2024-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142390825","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

RETRACTION: PNU-74654 enhances the antiproliferative effects of 5-FU in breast cancer and antagonizes thrombin-induced cell growth via the Wnt pathway. 返回：PNU-74654 可增强 5-FU 对乳腺癌的抗增殖作用，并通过 Wnt 通路拮抗凝血酶诱导的细胞生长。

IF 4.5 2区生物学

Journal of Cellular Physiology Pub Date : 2024-10-07 DOI: 10.1002/jcp.31462

{"title":"RETRACTION: PNU-74654 enhances the antiproliferative effects of 5-FU in breast cancer and antagonizes thrombin-induced cell growth via the Wnt pathway.","authors":"","doi":"10.1002/jcp.31462","DOIUrl":"https://doi.org/10.1002/jcp.31462","url":null,"abstract":"Retraction: F. Rahmani, F. Amerizadeh, S. M. Hassanian, M. Hashemzehi, S.-N. Nasiri, H. Fiuji, G. A. Ferns, M. Khazaei, and A. Avan, \"PNU-74654 Enhances the Antiproliferative Effects of 5-FU in Breast Cancer and Antagonizes Thrombin-induced Cell Growth via the Wnt Pathway,\" Journal of Cellular Physiology 234, no. 8 (2019): 14123-14132, https://doi.org/10.1002/jcp.28104. The above article, published online on 11 January 2019 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Robert Heath; and Wiley Periodicals LLC. The retraction has been agreed due to concerns raised by a third party on the data presented in the article. Specifically, image elements in Figure 1c were previously published by the same author group in a different scientific context. Additionally, the panels representing the histological staining corresponding to the \"Control\" and \"5-FU\" groups in Figure 3b were found to originate from the same biological sample. Finally, splicing sites have been detected within Figure 6b. The concerns were not satisfactorily addressed by the authors upon request. Accordingly, retraction is warranted as the editors have lost trust in the data presented in the article and in its conclusions. The corresponding author Majid Khazaei disagrees with the decision of retraction. No confirmation was obtained by the remaining co-authors.","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":" ","pages":"e31462"},"PeriodicalIF":4.5,"publicationDate":"2024-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142390827","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0