JOURNAL OF CELLULAR AND MOLECULAR MEDICINE最新文献

{"title":"Correction to “Protectin DX Promotes Epithelial Injury Repair and Inhibits Fibroproliferation Partly via ALX/PI3K Signalling Pathway”","authors":"","doi":"10.1111/jcmm.71087","DOIUrl":"10.1111/jcmm.71087","url":null,"abstract":"<p>J. X. Yang, M. Li, X. Hu, et al., “Protectin DX Promotes Epithelial Injury Repair and Inhibits Fibroproliferation Partly via ALX/PI3K Signalling Pathway,” <i>Journal of Cellular and Molecular Medicine</i> 24, no. 23 (2020): 14001–14012, https://doi.org/10.1111/jcmm.16011</p><p>In Yang JX et al., Figure 3 was incorrect due to an error in the preparation of this figure for publication. In Figure 3B, Figure 3C of the published article, panels from the PDX 36h group were incorrectly placed to represent the PDX 10nM group and the PDX+BOC-2 group separately due to mistakes during figure assembly. The corrected Figure 3 appears below. We apologize for any confusion this may have caused.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"30 5","pages":""},"PeriodicalIF":4.2,"publicationDate":"2026-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12973321/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147389470","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to “4-Octyl Itaconate Alleviates Cisplatin-Induced Ferroptosis Possibly via Activating the NRF2/HO-1 Signaling Pathway”","authors":"","doi":"10.1111/jcmm.71086","DOIUrl":"10.1111/jcmm.71086","url":null,"abstract":"<p>L. Zhang, W. Song, H. Li, et al., “4-octyl Itaconate Alleviates Cisplatin-Induced Ferroptosis Possibly via Activating the NRF2/HO-1 Signalling Pathway,” <i>Journal of Cellular and Molecular Medicine</i> 28, no. 7 (2024): e18207. https://doi.org/10.1111/jcmm.18207</p><p>In Figure S2C, the DAPI image of the cochlear Apical in the cisplatin-treated group does not correspond to the DAPI channel (blue) in the final merged image. This error occurred due to a mistake during image layout arrangement. The correct layout is shown below. We would like to emphasize that this error does not affect any of the study's findings or final conclusions, and it allows for any reproducibility experiments to confirm the results.</p><p>We sincerely apologize for any inconvenience caused to the readers and the publisher.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"30 5","pages":""},"PeriodicalIF":4.2,"publicationDate":"2026-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12973324/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147389548","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Brain-Targeting Curcumin Analog Inhibits Glioblastoma Progression Through THBS1/TGF-β1/PI3K–AKT Axis Modulation: Evidence From Experimental and Bioinformatic Analyses","authors":"Zijian Han,&nbsp;Xuetao Li,&nbsp;Yang Zhu,&nbsp;Zhimin Wang,&nbsp;Yingbo Hou,&nbsp;Huiling Tao,&nbsp;Meng Ma,&nbsp;Xiangtong Xie,&nbsp;HaiYang Zhang","doi":"10.1111/jcmm.71065","DOIUrl":"10.1111/jcmm.71065","url":null,"abstract":"<p>Glioblastoma (GBM) is the most aggressive primary brain tumour, associated with a dismal prognosis and an urgent need for innovative therapeutic strategies. To address this challenge, our group developed DMC-GF, a novel brain-targeted curcumin analog engineered to enhance blood–brain barrier permeability by blocking metabolic sites and improving GLUT1 recognition. Although its activity against glioma stem cells has been reported, the direct mechanisms by which DMC-GF acts on GBM cells remain unclear. In this study, we systematically investigated the molecular actions of DMC-GF using phenotypic assays, transcriptome sequencing, and bioinformatics analysis. DMC-GF exerted dose-dependent inhibitory effects on GBM cell proliferation, migration and invasion and concurrently promoted apoptosis, as reflected by reduced Bcl-2 expression, activation of Bax/Caspase-3 and reversal of epithelial–mesenchymal transition (E-cadherin↑, N-cadherin↓, MMP-3↓). Transcriptomic profiling identified THBS1 as a key downstream target, showing marked suppression following DMC-GF treatment. Functional experiments further confirmed that THBS1 knockdown mimics the anti-tumour effects of DMC-GF, whereas THBS1 overexpression partially mitigates its inhibitory actions. Mechanistic studies revealed that DMC-GF suppresses the non-canonical, Smad-independent TGF-β1 pathway by downregulating THBS1, thereby inhibiting PI3K/AKT signalling, as reflected by reduced phosphorylation of AKT, GSK3β and mTOR. Collectively, this work provides the first evidence that DMC-GF exerts anti-GBM effects through modulation of the THBS1/TGF-β1/PI3K-AKT axis. These findings suggest DMC-GF as a compelling brain-targeted therapeutic candidate, providing new mechanistic insights and a potential clinical strategy to overcome therapeutic resistance in GBM.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"30 5","pages":""},"PeriodicalIF":4.2,"publicationDate":"2026-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12975647/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147433102","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ODC1 Polyamine Metabolism Drives Prostate Cancer via AKT and Splicing","authors":"Jian Ma,&nbsp;Ting Pan,&nbsp;Shengli Sun,&nbsp;Musitapa Mutalifu,&nbsp;Wei Yang,&nbsp;Yue Niu,&nbsp;Peng Chen","doi":"10.1111/jcmm.71084","DOIUrl":"10.1111/jcmm.71084","url":null,"abstract":"<p>Prostate cancer is an aggressive disease with limited quantifiable biomarkers. One gene of interest is ODC1, which encodes ornithine decarboxylase, the rate-limiting enzyme converting ornithine to putrescine in polyamine metabolism. Although ODC1 is known to be involved in prostate cancer development, exactly how it drives the disease mechanistically is not fully understood. To explore this, we created a prostate cancer cell model with reduced ODC1 expression and examined its effects on tumour behaviours. Knocking down ODC1 significantly slowed cell growth and movement while increasing cell death. Using RNA sequencing, we identified over one thousand differentially expressed genes, with 565 upregulated and 497 downregulated, primarily linked to angiogenesis and cell adhesion. We also found more than two thousand alternative splicing events connected to cell cycle regulation and protein modification. Notably, genes including CAV1, ITGB1, BNIP3, and YTHDF2 were associated with the AKT signalling pathway, suggesting a functional link between ODC1 activity and cancer progression. These results indicate that ODC1 influences prostate cancer cell behaviour by regulating both gene expression and splicing, particularly affecting pathways involved in angiogenesis, adhesion, and the cell cycle. This points to the AKT pathway and polyamine metabolism as potentially valuable targets for future prostate cancer therapies.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"30 5","pages":""},"PeriodicalIF":4.2,"publicationDate":"2026-03-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12971389/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147389677","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Jianpi Jiedu Xiaozheng Fang Regulates Hepatocellular Carcinoma Proliferation and Metastasis Based on Network Pharmacology","authors":"Bin Li,&nbsp;Han-Qian Shi,&nbsp;Rui Luo,&nbsp;Zi-Qi Zhang,&nbsp;Xiao-Chen Dong,&nbsp;Xiao-Hua Li,&nbsp;Shi-Qin Ye,&nbsp;Chong Zhong","doi":"10.1111/jcmm.71040","DOIUrl":"10.1111/jcmm.71040","url":null,"abstract":"<p>Hepatocellular carcinoma (HCC) is a primary malignant tumour that impacts patients' quality of life. Currently, clinical experience from The First Affiliated Hospital of Guangzhou University of Chinese Medicine suggests that Jianpi Jiedu Xiaozheng Fang (JPJDXZF) demonstrates promising efficacy in the treatment of HCC. We aimed to explore the mechanisms of JPJDXZF in HCC based on network pharmacology. The components and their relevant targets of JPJDXZF were identified using databases such as SymMap, TCMID, TCMSP, and TCM-ID. Following ADME screening, 1443 active components of JPJDXZF were identified, and 435 corresponding drug targets were predicted using the SwissTargetPrediction database. Subsequently, prognosis-related differentially expressed genes (DEGs) associated with HCC were analyzed using TCGA and GTEx datasets, and a gene expression matrix was derived. Key genes involved in HCC regulation were identified, and functional analyses were performed. Furthermore, we explored the regulatory effects of JPJDXZF at the cellular, organoid, and animal levels. We identified 18 intersecting genes between HCC prognosis-related genes and JPJDXZF-target genes. Venn diagram analysis successfully identified BIRC5 and CYP2E1 as two potential targets for JPJDXZF in treating HCC. Pathway enrichment analysis indicated that the core targets of JPJDXZF were enriched in multiple signalling pathways, including the Hippo pathway, in which BIRC5 is involved as a downstream regulatory gene. In in vitro experiments, JPJDXZF-containing serum significantly reduced the viability and migration of HepG2 and MHCC97-H cells, leading to a decrease in organoid diameter and ATP activity in HCC organoids. In in vivo experiments, tumours in nude mice treated with JPJDXZF exhibited reduced volume and weight, along with decreased expression of BIRC5 and Hippo pathway effectors YAP and TAZ. At the mechanistic level, JPJDXZF treatment was associated with altered Hippo pathway–related signalling, accompanied by reduced YAP/TAZ activity and changes in BIRC5 expression, together with effects on HCC cell proliferation and apoptosis. In addition, siMST1/2 interference and EMT inhibitor-1 treatment partially attenuated the effects of JPJDXZF on cell viability, migration, and apoptosis. JPJDXZF regulates BIRC5 expression in association with Hippo pathway activity in HCC. In vitro, in vivo, and molecular mechanism analyses support JPJDXZF as a potential therapeutic strategy for HCC by modulating key proteins in the Hippo pathway, thus affecting HCC cell proliferation, apoptosis, and migration.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"30 5","pages":""},"PeriodicalIF":4.2,"publicationDate":"2026-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12967627/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147372612","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bioengineered AAV9 and Optimised Microdystrophin Vectors Augment Phenotypic Rescue in a Murine Model of Duchenne Muscular Dystrophy","authors":"Mohankumar B. Senthilkumar,&nbsp;Sanya Sharma,&nbsp;Navaneeth Srinivasan,&nbsp;Anila Varghese,&nbsp;Pratiksha Sarangi,&nbsp;Vijayata Singh,&nbsp;Narendra Kumar,&nbsp;Devyani Yenurkar,&nbsp;Sudip Mukherjee,&nbsp;Sonal Amit,&nbsp;Sameer Bhatia,&nbsp;Santosh K. Misra,&nbsp;Ratna Dua Puri,&nbsp;Jeffrey Chamberlain,&nbsp;Giridhara R. Jayandharan","doi":"10.1111/jcmm.71078","DOIUrl":"10.1111/jcmm.71078","url":null,"abstract":"<p>Duchenne muscular dystrophy (DMD) is a severe neuromuscular disorder without an effective cure. Adeno-associated virus (AAV) based gene therapy has improved dystrophin function, with sub-optimal clinical outcomes. We reasoned that a combination of rational engineering of AAV9 capsids modified at the post-translational modification sites, optimal promoter selection, and codon-optimisation of the microdystrophin (μDys) can enhance the AAV9 vector functionality. Our initial promoter screening demonstrated improved dystrophin expression in muscle fibres with a ubiquitous CAG promoter (1.61-fold in CAG vs. MHCK7, <i>p</i> &lt; 0.0001) in <i>mdx</i> mice. We then evaluated two engineered AAV9 capsids (N57Q, K51Q) containing CAG-μDys intramuscularly in vivo, which demonstrated a significant improvement in grip strength 18 weeks after gene therapy. Subsequent evaluation of a codon-optimised microdystrophin transgene under the control of the optimal CAG promoter and capsid (AAV9K51Q) by intramuscular administration revealed enhanced muscle grip strength and dystrophin-glycoprotein complex restoration up to 4 months after gene therapy. Based on the improved performance of AAV9K51Q vectors during intramuscular gene transfer, we performed a systemic administration of these vectors alone, and a comparison with the control group revealed a significantly increased muscle contraction force by 1.6–1.7 fold and a 30%–60% dystrophin restoration in skeletal and cardiac muscles, up to 14 months after gene therapy. Collectively, our study underscores the therapeutic potential of engineered AAV9 vectors for potential clinical application in patients with DMD.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"30 5","pages":""},"PeriodicalIF":4.2,"publicationDate":"2026-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12966934/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147369211","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"HBx Promotes Liver Cancer Cells to Escape NK-92 Cell Attack by Mediating ADAM10 to Enzyme Cut MICA/B Shedding From Cancer Cell Membrane","authors":"Kailin Huang,&nbsp;Qiushi Yin,&nbsp;Xueqin Wu,&nbsp;Kun Liu,&nbsp;Bo Lin,&nbsp;Wei Li,&nbsp;Yinglian Pan,&nbsp;Mingyue Zhu,&nbsp;Mengsen Li","doi":"10.1111/jcmm.71081","DOIUrl":"10.1111/jcmm.71081","url":null,"abstract":"<p>MICA/B shedding from the membrane of cancer cells can inhibit natural killer (NK) cells from attacking hepatocellular carcinoma (HCC). This study explored the role of HBx in mediating MICA/B shedding. The expression of HBx, MICA/B and HIF-1α in HBV-infected HCC was analysed using bioinformatics, and the localization of these proteins in tissues was verified using immunohistochemistry and immunofluorescence. HBx-related signalling pathways were screened using RNA sequencing and KEGG pathway enrichment analyses. The expression of ADAM10 and MICA/B was detected by Western blotting, and the dynamic changes of MICA/B in the membrane and supernatant were evaluated by flow cytometry and ELISA. The HIF-1α inhibitor (LW-6) and ADAM10 inhibitor (GI254023X) were used to treat the HCC cells. The killing effect of NK-92 cells on HCC cells was evaluated using lactate dehydrogenase release, cytotoxicity assays, clone formation and live-cell imaging, and the secretion levels of IFN-γ, IL-2 and IL-10 were measured. These results indicated that HBx, MICA/B and HIF-1α were highly expressed in HBV-infected HCC tissues. HBx promotes shedding of MICA/B from HCC cell membranes by upregulating the activity of ADAM10. LW-6 reversed the induction effect of HBx on ADAM10 and GI254023X significantly restored MICA/B levels on the membrane surface of HCC cells. Overexpression of HBx increases the resistance of HCC cells to NK-92 cells and inhibits the secretion of IFN-γ, IL-2 and IL-10. In conclusion, HBx regulates the expression of ADAM10 by activating the HIF-1α signalling pathway. ADAM10 cuts MICA/B shedding from the membrane surface of HCC cells, resulting in escape attack by NK-92 cells.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"30 5","pages":""},"PeriodicalIF":4.2,"publicationDate":"2026-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12965905/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147369308","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Calcium Dysregulation Promotes Glioma Progression by Inhibiting STAT3 Degradation Through Blocking Chaperone-Mediated Autophagy","authors":"Jialong Chen,&nbsp;Yixi Lai,&nbsp;Mingque Li,&nbsp;ZiWei Cai,&nbsp;Renjian Lu,&nbsp;Linhua Liu,&nbsp;Yongming Peng,&nbsp;Chunlai Fu,&nbsp;Zhefan Xie,&nbsp;Xueqion Zhou,&nbsp;Jiaxian Liu,&nbsp;He Zhang","doi":"10.1111/jcmm.71062","DOIUrl":"10.1111/jcmm.71062","url":null,"abstract":"<p>Calcium dysregulation is closely associated with cancer cell proliferation, migration, and invasion. Transient receptor potential canonical 1 (TRPC1) plays an essential role in regulating calcium homeostasis. However, the role of TRPC1 in calcium dysregulation in gliomas remains incompletely understood. In this study, we demonstrate that TRPC1 promotes glioma cell migration by increasing Signal transduction and transcription activator 3 (STAT3) protein levels. Furthermore, we show that TRPC1 modulates STAT3 stability by inhibiting chaperone-mediated autophagy (CMA), and we identify STAT3 as a novel substrate of CMA. Additionally, TRPC1 modulates the interaction between HDAC6 and Heat Shock Cognate 70 through intracellular Ca²⁺ homeostasis, which is associated with changes in CMA activity. These changes prevent STAT3 degradation, highlighting the TRPC1-HDAC6 axis as a regulator of glioma progression. Thus, the TRPC1-HDAC6 axis inhibits STAT3 degradation by suppressing CMA activity, contributing to glioma progression. This pathway may represent a potential therapeutic target.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"30 5","pages":""},"PeriodicalIF":4.2,"publicationDate":"2026-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12963025/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147365298","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to ‘Quercetin Can Be a More Reliable Treatment for Metastatic Prostate Cancer Than the Localized Disease: An In Vitro Study’","authors":"","doi":"10.1111/jcmm.71009","DOIUrl":"10.1111/jcmm.71009","url":null,"abstract":"<p>A. Mirzaei, R. Deyhimfar, H. Azodian Ghajar, R. Mashhadi, M. Noori, H. Dialameh, Z. Aghsaeifard, and S. M. Aghamir, ‘Quercetin Can Be a More Reliable Treatment for Metastatic Prostate Cancer Than the Localized Disease: An In Vitro Study,’ <i>Journal of Cellular and Molecular Medicine</i> 27, no. 12 (2023): 1725–1734.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"30 5","pages":""},"PeriodicalIF":4.2,"publicationDate":"2026-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12960733/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147355382","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RETRACTION: EZH2 Promotes Invasion and Tumour Glycolysis by Regulating STAT3 and FoxO1 Signalling in Human OSCC Cells","authors":"","doi":"10.1111/jcmm.71083","DOIUrl":"10.1111/jcmm.71083","url":null,"abstract":"<p>\u0000 <b>RETRACTION</b>: <span>M. Zheng</span>, <span>M.-X. Cao</span>, <span>X.-J. Luo</span>, <span>L. Li</span>, <span>K. Wang</span>, <span>S.-S. Wang</span>, <span>H.-F. Wang</span>, <span>Y.-J. Tang</span>, <span>Y.-L. Tang</span>, <span>X.-H. Liang</span>, “ <span>EZH2 Promotes Invasion and Tumour Glycolysis by Regulating STAT3 and FoxO1 Signalling in Human OSCC Cells</span>,” <i>Journal of Cellular and Molecular Medicine</i> <span>23</span>, no. <span>10</span> (<span>2019</span>): <span>6942</span>–<span>6954</span>, https://doi.org/10.1111/jcmm.14579.\u0000 </p><p>The above article, published online on 31 July 2019 in Wiley Online Library (wileyonlinelibrary.com) has been retracted by agreement between the journal Editor-in-Chief, Stefan N. Constantinescu; The Foundation for Cellular and Molecular Medicine; and John Wiley and Sons Ltd. The retraction has been agreed due to concerns raised by third parties. Specifically, instances of image duplication have been identified between Figures 2C and 3C, between Figures 2A and 3A, and between Figures 2D and 5A. Furthermore, image elements in Figures 2C and 3C have been published previously by the same author group in a different scientific context. The clarification provided by the authors was insufficient to adequately address the concerns raised, as additional inaccuracies were identified by the authors during their review of the original data. Accordingly, the article has been retracted, as the editors no longer have confidence in the overall reliability of the data or in the conclusions presented in the article. The authors have been informed of the retraction decision but were not available for final confirmation.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"30 5","pages":""},"PeriodicalIF":4.2,"publicationDate":"2026-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12958479/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147355397","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}