Pub Date : 2024-04-01Epub Date: 2024-02-09DOI: 10.3892/ijmm.2024.5355
Feng Yuan, Zhiping Lou, Zhifeng Zhou, Xiaojun Yan
Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that the colony formation assay data shown in Figs. 4C and 6D and the Transwell migration and invasion assay data shown in Figs. 4D, 6E and 6F were strikingly similar to data appearing in different form in other research articles written by different authors at different research institutes that had either already been published, or were submitted for publication at around the same time. Owing to the fact that contentious data in the above article had already been published elsewhere prior to its submission to International Journal of Molecular Medicine, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Molecular Medicine 47: 54, 2021; DOI: 10.3892/ijmm.2021.4887].
{"title":"[Retracted] Long non‑coding RNA KCNQ1OT1 promotes nasopharyngeal carcinoma cell cisplatin resistance via the miR‑454/USP47 axis.","authors":"Feng Yuan, Zhiping Lou, Zhifeng Zhou, Xiaojun Yan","doi":"10.3892/ijmm.2024.5355","DOIUrl":"10.3892/ijmm.2024.5355","url":null,"abstract":"<p><p>Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that the colony formation assay data shown in Figs. 4C and 6D and the Transwell migration and invasion assay data shown in Figs. 4D, 6E and 6F were strikingly similar to data appearing in different form in other research articles written by different authors at different research institutes that had either already been published, or were submitted for publication at around the same time. Owing to the fact that contentious data in the above article had already been published elsewhere prior to its submission to <i>International Journal of Molecular Medicine</i>, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Molecular Medicine 47: 54, 2021; DOI: 10.3892/ijmm.2021.4887].</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":null,"pages":null},"PeriodicalIF":5.4,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10903928/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139706710","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-04-01Epub Date: 2024-02-23DOI: 10.3892/ijmm.2024.5360
Jiaqi Guo, Jun Wang, Pei Liang, E Tian, Dan Liu, Zhaoqi Guo, Jingyu Chen, Yuejin Zhang, Zhanghong Zhou, Weijia Kong, Debbie C Crans, Yisheng Lu, Sulin Zhang
The vestibular system may have a critical role in the integration of sensory information and the maintenance of cognitive function. A dysfunction in the vestibular system has a significant impact on quality of life. Recent research has provided evidence of a connection between vestibular information and cognitive functions, such as spatial memory, navigation and attention. Although the exact mechanisms linking the vestibular system to cognition remain elusive, researchers have identified various pathways. Vestibular dysfunction may lead to the degeneration of cortical vestibular network regions and adversely affect synaptic plasticity and neurogenesis in the hippocampus, ultimately contributing to neuronal atrophy and cell death, resulting in memory and visuospatial deficits. Furthermore, the extent of cognitive impairment varies depending on the specific type of vestibular disease. In the present study, the current literature was reviewed, potential causal relationships between vestibular dysfunction and cognitive performance were discussed and directions for future research were proposed.
{"title":"Vestibular dysfunction leads to cognitive impairments: State of knowledge in the field and clinical perspectives (Review).","authors":"Jiaqi Guo, Jun Wang, Pei Liang, E Tian, Dan Liu, Zhaoqi Guo, Jingyu Chen, Yuejin Zhang, Zhanghong Zhou, Weijia Kong, Debbie C Crans, Yisheng Lu, Sulin Zhang","doi":"10.3892/ijmm.2024.5360","DOIUrl":"10.3892/ijmm.2024.5360","url":null,"abstract":"<p><p>The vestibular system may have a critical role in the integration of sensory information and the maintenance of cognitive function. A dysfunction in the vestibular system has a significant impact on quality of life. Recent research has provided evidence of a connection between vestibular information and cognitive functions, such as spatial memory, navigation and attention. Although the exact mechanisms linking the vestibular system to cognition remain elusive, researchers have identified various pathways. Vestibular dysfunction may lead to the degeneration of cortical vestibular network regions and adversely affect synaptic plasticity and neurogenesis in the hippocampus, ultimately contributing to neuronal atrophy and cell death, resulting in memory and visuospatial deficits. Furthermore, the extent of cognitive impairment varies depending on the specific type of vestibular disease. In the present study, the current literature was reviewed, potential causal relationships between vestibular dysfunction and cognitive performance were discussed and directions for future research were proposed.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":null,"pages":null},"PeriodicalIF":5.4,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10914312/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139930985","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Phospholipids (PLs) are principle constituents of biofilms, with their fatty acyl chain composition significantly impacting the biophysical properties of membranes, thereby influencing biological processes. Recent studies have elucidated that fatty acyl chains, under the enzymatic action of lyso‑phosphatidyl‑choline acyltransferases (LPCATs), expedite incorporation into the sn‑2 site of phosphatidyl‑choline (PC), profoundly affecting pathophysiology. Accumulating evidence suggests that alterations in LPCAT activity are implicated in various diseases, including non‑alcoholic fatty liver disease (NAFLD), hepatitis C, atherosclerosis and cancer. Specifically, LPCAT3 is instrumental in maintaining systemic lipid homeostasis through its roles in hepatic lipogenesis, intestinal lipid absorption and lipoprotein secretion. The liver X receptor (LXR), pivotal in lipid homeostasis, modulates cholesterol, fatty acid (FA) and PL metabolism. LXR's capacity to modify PL composition in response to cellular sterol fluctuations is a vital mechanism for protecting biofilms against lipid stress. Concurrently, LXR activation enhances LPCAT3 expression on cell membranes and elevates polyunsaturated PL levels. This activation can ameliorate saturated free FA effects in vitro or endoplasmic reticulum stress in vivo due to lipid accumulation in hepatic cells. Pharmacological interventions targeting LXR, LPCAT and membrane PL components could offer novel therapeutic directions for NAFLD management. The present review primarily focused on recent advancements in understanding the LPCAT3 signaling pathway's role in lipid metabolism related to NAFLD, aiming to identify new treatment targets for the disease.
{"title":"Research progress, challenges and perspectives of phospholipids metabolism in the LXR‑LPCAT3 signaling pathway and its relation to NAFLD (Review).","authors":"Junmin Wang, Jiacheng Li, Yugang Fu, Yingying Zhu, Liubing Lin, Yong Li","doi":"10.3892/ijmm.2024.5356","DOIUrl":"10.3892/ijmm.2024.5356","url":null,"abstract":"<p><p>Phospholipids (PLs) are principle constituents of biofilms, with their fatty acyl chain composition significantly impacting the biophysical properties of membranes, thereby influencing biological processes. Recent studies have elucidated that fatty acyl chains, under the enzymatic action of lyso‑phosphatidyl‑choline acyltransferases (LPCATs), expedite incorporation into the sn‑2 site of phosphatidyl‑choline (PC), profoundly affecting pathophysiology. Accumulating evidence suggests that alterations in LPCAT activity are implicated in various diseases, including non‑alcoholic fatty liver disease (NAFLD), hepatitis C, atherosclerosis and cancer. Specifically, LPCAT3 is instrumental in maintaining systemic lipid homeostasis through its roles in hepatic lipogenesis, intestinal lipid absorption and lipoprotein secretion. The liver X receptor (LXR), pivotal in lipid homeostasis, modulates cholesterol, fatty acid (FA) and PL metabolism. LXR's capacity to modify PL composition in response to cellular sterol fluctuations is a vital mechanism for protecting biofilms against lipid stress. Concurrently, LXR activation enhances LPCAT3 expression on cell membranes and elevates polyunsaturated PL levels. This activation can ameliorate saturated free FA effects <i>in vitro</i> or endoplasmic reticulum stress <i>in vivo</i> due to lipid accumulation in hepatic cells. Pharmacological interventions targeting LXR, LPCAT and membrane PL components could offer novel therapeutic directions for NAFLD management. The present review primarily focused on recent advancements in understanding the LPCAT3 signaling pathway's role in lipid metabolism related to NAFLD, aiming to identify new treatment targets for the disease.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":null,"pages":null},"PeriodicalIF":5.4,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10903931/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139740916","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-04-01Epub Date: 2024-03-01DOI: 10.3892/ijmm.2024.5364
Wenlin Yang, Yingze Wei, Ting Wang, Ying Xu, Xiaoxia Jin, Hongyan Qian, Shuyun Yang, Song He
SET domain bifurcated 1 (SETDB1), a pivotal histone lysine methyltransferase, is transported to the cytoplasm via a chromosome region maintenance 1 (CMR1)‑dependent pathway, contributing to non‑histone methylation. However, the function and underlying mechanism of cytoplasmic SETDB1 in breast cancer remain elusive. In the present study, immunohistochemistry revealed that elevated cytoplasmic SETDB1 was correlated with lymph node metastasis and more aggressive breast cancer subtypes. Functionally, wound healing and Transwell assays showed that cytoplasmic SETDB1 is key for cell migration and invasion, as well as induction of epithelial‑mesenchymal transition (EMT), which was reversed by leptomycin B (LMB, a CMR1 inhibitor) treatment. Furthermore, RNA‑seq and metabolite detection revealed that cytoplasmic SETDB1 was associated with metabolism pathway and elevated levels of metabolites involved in the Warburg effect, including glucose, pyruvate, lactate and ATP. Immunoblotting and reverse transcription‑quantitative PCR verified that elevation of cytoplasmic SETDB1 contributed to elevation of c‑MYC expression and subsequent upregulation of lactate dehydrogenase A (LDHA) expression. Notably, gain‑ and loss‑of‑function approaches revealed that LDHA overexpression in T47D cells enhanced migration and invasion by inducing EMT, while its depletion in SETDB1‑overexpressing MCF7 cells reversed SETDB1‑induced migration and invasion, as well as the Warburg effect and EMT. In conclusion, subcellular localization of cytoplasmic SETDB1 may be a pivotal factor in breast cancer progression. The present study offers valuable insight into the novel functions and mechanisms of cytoplasmic SETDB1.
{"title":"Cytoplasmic localization of SETDB1‑induced Warburg effect via c‑MYC‑LDHA axis enhances migration and invasion in breast carcinoma.","authors":"Wenlin Yang, Yingze Wei, Ting Wang, Ying Xu, Xiaoxia Jin, Hongyan Qian, Shuyun Yang, Song He","doi":"10.3892/ijmm.2024.5364","DOIUrl":"10.3892/ijmm.2024.5364","url":null,"abstract":"<p><p>SET domain bifurcated 1 (SETDB1), a pivotal histone lysine methyltransferase, is transported to the cytoplasm via a chromosome region maintenance 1 (CMR1)‑dependent pathway, contributing to non‑histone methylation. However, the function and underlying mechanism of cytoplasmic SETDB1 in breast cancer remain elusive. In the present study, immunohistochemistry revealed that elevated cytoplasmic SETDB1 was correlated with lymph node metastasis and more aggressive breast cancer subtypes. Functionally, wound healing and Transwell assays showed that cytoplasmic SETDB1 is key for cell migration and invasion, as well as induction of epithelial‑mesenchymal transition (EMT), which was reversed by leptomycin B (LMB, a CMR1 inhibitor) treatment. Furthermore, RNA‑seq and metabolite detection revealed that cytoplasmic SETDB1 was associated with metabolism pathway and elevated levels of metabolites involved in the Warburg effect, including glucose, pyruvate, lactate and ATP. Immunoblotting and reverse transcription‑quantitative PCR verified that elevation of cytoplasmic SETDB1 contributed to elevation of c‑MYC expression and subsequent upregulation of lactate dehydrogenase A (LDHA) expression. Notably, gain‑ and loss‑of‑function approaches revealed that LDHA overexpression in T47D cells enhanced migration and invasion by inducing EMT, while its depletion in SETDB1‑overexpressing MCF7 cells reversed SETDB1‑induced migration and invasion, as well as the Warburg effect and EMT. In conclusion, subcellular localization of cytoplasmic SETDB1 may be a pivotal factor in breast cancer progression. The present study offers valuable insight into the novel functions and mechanisms of cytoplasmic SETDB1.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":null,"pages":null},"PeriodicalIF":5.4,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10914311/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139996228","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Yi Wei, Li Li, Yiping Wang, Yan Chen, Zhengyang Li, Chufei Huang, Yangchen Wei, Chiyu Jia, Zuo Wang, Junlin Liao
Pyroptosis, a programmed cell death marked by lytic and inflammatory characteristics, plays a crucial role in non‑infectious inflammation‑related diseases but can lead to detrimental outcomes when dysregulated. Stem cells have emerged as key players in modulating pyroptosis through paracrine signaling, offering a novel avenue for tissue repair and regeneration. The present review delved into previous studies elucidating the intricate interplay between stem cells and pyroptosis, emphasizing the potential of stem cell‑based therapies in regulating pyroptotic pathways. The exploration of this dynamic interaction holds promise for developing strategies to harness stem cells for effective tissue repair and regeneration in the context of inflammation‑related diseases.
{"title":"Stem cell‑mediated modulation of pyroptosis contributes to tissue repair in noninfective inflammatory‑related diseases (Review).","authors":"Yi Wei, Li Li, Yiping Wang, Yan Chen, Zhengyang Li, Chufei Huang, Yangchen Wei, Chiyu Jia, Zuo Wang, Junlin Liao","doi":"10.3892/ijmm.2024.5370","DOIUrl":"https://doi.org/10.3892/ijmm.2024.5370","url":null,"abstract":"Pyroptosis, a programmed cell death marked by lytic and inflammatory characteristics, plays a crucial role in non‑infectious inflammation‑related diseases but can lead to detrimental outcomes when dysregulated. Stem cells have emerged as key players in modulating pyroptosis through paracrine signaling, offering a novel avenue for tissue repair and regeneration. The present review delved into previous studies elucidating the intricate interplay between stem cells and pyroptosis, emphasizing the potential of stem cell‑based therapies in regulating pyroptotic pathways. The exploration of this dynamic interaction holds promise for developing strategies to harness stem cells for effective tissue repair and regeneration in the context of inflammation‑related diseases.","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":null,"pages":null},"PeriodicalIF":5.4,"publicationDate":"2024-03-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140365721","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-03-01Epub Date: 2024-01-19DOI: 10.3892/ijmm.2024.5350
Xinwang Zhu, Congxiao Zhang, Linlin Liu, Li Xu, Li Yao
The senolytics dasatinib and quercetin (DQ) alleviate age‑related disorders. However, limited information is available regarding the effects of DQ on diabetic kidney disease (DKD). The present study aimed to explore the effects of DQ on DKD and its potential molecular mechanism(s). Dasatinib (5 mg/kg) and quercetin (50 mg/kg) were administered to diabetic db/db mice by gavage for 20 weeks. Body weight, urine albumin‑creatinine ratio (ACR), serum creatinine (Scr), and blood urea nitrogen (BUN) were recorded at the indicated time periods. Periodic acid‑Schiff and Masson's staining were performed to assess the histopathological changes of kidney tissues. Immunohistochemical analysis, immunofluorescence and western blotting were performed to evaluate the expression levels of extracellular matrix (ECM) proteins, autophagic and podocyte differentiation‑related proteins. In addition, mouse podocytes were administered with high‑glucose, DQ and 3‑methyladenine (3‑MA), and the expression levels of autophagic and podocyte differentiation‑related proteins were measured. Moreover, following overexpression of the Notch intracellular domain (NICD), the expression levels of NICD, autophagic and podocyte differentiation‑related proteins were further assessed. DQ significantly reduced the body weight, blood glucose, ACR, Scr and BUN levels and improved the histopathological changes induced in diabetic db/db mice. In addition, DQ caused a significant downregulation of the expression levels of the ECM proteins, improved autophagy and induced an upregulation of the expression levels of podocyte differentiation‑related proteins. Administration of 3‑MA to mice significantly reduced podocyte differentiation, and overexpression of NICD could reverse the effects of DQ on autophagy and podocyte differentiation in vitro. The present study suggests that DQ protects against DKD by activation of autophagy to alleviate podocyte dedifferentiation via the Notch pathway.
{"title":"Senolytic combination of dasatinib and quercetin protects against diabetic kidney disease by activating autophagy to alleviate podocyte dedifferentiation via the Notch pathway.","authors":"Xinwang Zhu, Congxiao Zhang, Linlin Liu, Li Xu, Li Yao","doi":"10.3892/ijmm.2024.5350","DOIUrl":"10.3892/ijmm.2024.5350","url":null,"abstract":"<p><p>The senolytics dasatinib and quercetin (DQ) alleviate age‑related disorders. However, limited information is available regarding the effects of DQ on diabetic kidney disease (DKD). The present study aimed to explore the effects of DQ on DKD and its potential molecular mechanism(s). Dasatinib (5 mg/kg) and quercetin (50 mg/kg) were administered to diabetic db/db mice by gavage for 20 weeks. Body weight, urine albumin‑creatinine ratio (ACR), serum creatinine (Scr), and blood urea nitrogen (BUN) were recorded at the indicated time periods. Periodic acid‑Schiff and Masson's staining were performed to assess the histopathological changes of kidney tissues. Immunohistochemical analysis, immunofluorescence and western blotting were performed to evaluate the expression levels of extracellular matrix (ECM) proteins, autophagic and podocyte differentiation‑related proteins. In addition, mouse podocytes were administered with high‑glucose, DQ and 3‑methyladenine (3‑MA), and the expression levels of autophagic and podocyte differentiation‑related proteins were measured. Moreover, following overexpression of the Notch intracellular domain (NICD), the expression levels of NICD, autophagic and podocyte differentiation‑related proteins were further assessed. DQ significantly reduced the body weight, blood glucose, ACR, Scr and BUN levels and improved the histopathological changes induced in diabetic db/db mice. In addition, DQ caused a significant downregulation of the expression levels of the ECM proteins, improved autophagy and induced an upregulation of the expression levels of podocyte differentiation‑related proteins. Administration of 3‑MA to mice significantly reduced podocyte differentiation, and overexpression of NICD could reverse the effects of DQ on autophagy and podocyte differentiation <i>in vitro</i>. The present study suggests that DQ protects against DKD by activation of autophagy to alleviate podocyte dedifferentiation via the Notch pathway.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":null,"pages":null},"PeriodicalIF":5.4,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10852012/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139491410","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-03-01Epub Date: 2024-01-26DOI: 10.3892/ijmm.2024.5351
Furong Song, Jun Liu, Yawei Feng, Yi Jin
Following the publication of the above article, an interested reader drew to the authors' attention that the western blots for the PCNA and cyclin D1 bands appeared to be strikingly similar. The authors were able to re‑examine their original data, and recognize how the error was made with respect to the compilation of this figure (they were also able to demonstrate to the Editorial Office how the error occurred). The revised version of Fig. 3, now incorporating the correct data for the PCNA bands in Fig. 3A, is shown on the next page. The authors can confirm that the errors associated with this figure did not have a significant impact on either the results or the conclusions reported in this study, and all the authors agree with the publication of this Corrigendum. The authors are grateful to the Editor of International Journal of Molecular Medicine for allowing them the opportunity to publish this Corrigendum; furthermore, they apologize to the readership of the Journal for any inconvenience caused. [International Journal of Molecular Medicine 46: 1135‑1145, 2020; DOI: 10.3892/ijmm.2020.4667].
上述文章发表后,一位感兴趣的读者提请作者注意,PCNA 和细胞周期蛋白 D1 带的 Western 印迹似乎惊人地相似。作者重新检查了他们的原始数据,并认识到在绘制该图时是如何出错的(他们还向编辑部证明了错误是如何发生的)。下一页是图 3 的修订版,其中包含了图 3A 中 PCNA 条带的正确数据。作者可以确认,与该图相关的错误并未对本研究报告的结果或结论产生重大影响,所有作者均同意发表本更正。作者感谢《国际分子医学杂志》编辑允许他们有机会发表本更正;此外,他们对给该杂志读者造成的不便深表歉意。[国际分子医学杂志》(International Journal of Molecular Medicine)46:1135-1145, 2020; DOI: 10.3892/ijmm.2020.4667]。
{"title":"[Corrigendum] Propofol‑induced HOXA11‑AS promotes proliferation, migration and invasion, but inhibits apoptosis in hepatocellular carcinoma cells by targeting miR‑4458.","authors":"Furong Song, Jun Liu, Yawei Feng, Yi Jin","doi":"10.3892/ijmm.2024.5351","DOIUrl":"10.3892/ijmm.2024.5351","url":null,"abstract":"<p><p>Following the publication of the above article, an interested reader drew to the authors' attention that the western blots for the PCNA and cyclin D1 bands appeared to be strikingly similar. The authors were able to re‑examine their original data, and recognize how the error was made with respect to the compilation of this figure (they were also able to demonstrate to the Editorial Office how the error occurred). The revised version of Fig. 3, now incorporating the correct data for the PCNA bands in Fig. 3A, is shown on the next page. The authors can confirm that the errors associated with this figure did not have a significant impact on either the results or the conclusions reported in this study, and all the authors agree with the publication of this Corrigendum. The authors are grateful to the Editor of <i>International Journal of Molecular Medicine</i> for allowing them the opportunity to publish this Corrigendum; furthermore, they apologize to the readership of the Journal for any inconvenience caused. [International Journal of Molecular Medicine 46: 1135‑1145, 2020; DOI: 10.3892/ijmm.2020.4667].</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":null,"pages":null},"PeriodicalIF":5.4,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10852010/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139563588","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-03-01Epub Date: 2024-01-12DOI: 10.3892/ijmm.2024.5347
Fanglu Zhong, Sheng Cao, Li Yang, Junbi Liu, Bin Gui, Hao Wang, Nan Jiang, Qing Zhou, Qing Deng
Diabetic wounds remain a great challenge for clinicians globally as a lack of effective radical treatment often results in poor prognosis. Exosomes derived from adipose‑derived stem cells (ADSC‑Exos) have been explored as an appealing nanodrug delivery system in the treatment of diabetic wounds. However, the short half‑life and low utilization efficiency of exosomes limit their therapeutic effects. Low‑intensity pulsed ultrasound (LIPUS) provides a non‑invasive mechanical stimulus to cells and exerts a number of biological effects such as cavitation and thermal effects. In the present study, whether LIPUS could enhance ADSC‑Exo‑mediated diabetic wound repair was investigated and its possible mechanism of action was explored. After isolation and characterization, ADSC‑Exos were injected into mice with diabetic wounds, then the mice were exposed to LIPUS irradiation. The control mice were subcutaneously injected with PBS. Wound healing assays, laser Doppler perfusion, Masson's staining and angiogenesis assays were used to assess treatment efficiency. Then, ADSC‑Exos were cocultured with human umbilical vein endothelial cells (HUVECs), and the proliferation, migration and tube formation of HUVECs were assessed. Moreover, the cellular uptake of ADSC‑Exos invitro and invivo was assessed to explore the synergistic mechanisms underlying the effects of LIPUS. The invivo results demonstrated that LIPUS increased the uptake of exosomes and prolonged the residence of exosomes in the wound area, thus enhancing angiogenesis and accelerating wound repair in diabetic mice. The invitro results further confirmed that LIPUS enhanced the uptake efficiency of ADSC‑Exos by 10.93‑fold and significantly increased the proliferation, migration and tubular formation of HUVECs. Therefore, the present study indicates that LIPUS is a promising strategy to improve the therapeutic effects of ADSC‑Exos in diabetic wounds by promoting the cellular uptake of exosomes and enhancing angiogenesis.
{"title":"Low‑intensity pulsed ultrasound accelerates diabetic wound healing by ADSC‑derived exosomes via promoting the uptake of exosomes and enhancing angiogenesis.","authors":"Fanglu Zhong, Sheng Cao, Li Yang, Junbi Liu, Bin Gui, Hao Wang, Nan Jiang, Qing Zhou, Qing Deng","doi":"10.3892/ijmm.2024.5347","DOIUrl":"10.3892/ijmm.2024.5347","url":null,"abstract":"<p><p>Diabetic wounds remain a great challenge for clinicians globally as a lack of effective radical treatment often results in poor prognosis. Exosomes derived from adipose‑derived stem cells (ADSC‑Exos) have been explored as an appealing nanodrug delivery system in the treatment of diabetic wounds. However, the short half‑life and low utilization efficiency of exosomes limit their therapeutic effects. Low‑intensity pulsed ultrasound (LIPUS) provides a non‑invasive mechanical stimulus to cells and exerts a number of biological effects such as cavitation and thermal effects. In the present study, whether LIPUS could enhance ADSC‑Exo‑mediated diabetic wound repair was investigated and its possible mechanism of action was explored. After isolation and characterization, ADSC‑Exos were injected into mice with diabetic wounds, then the mice were exposed to LIPUS irradiation. The control mice were subcutaneously injected with PBS. Wound healing assays, laser Doppler perfusion, Masson's staining and angiogenesis assays were used to assess treatment efficiency. Then, ADSC‑Exos were cocultured with human umbilical vein endothelial cells (HUVECs), and the proliferation, migration and tube formation of HUVECs were assessed. Moreover, the cellular uptake of ADSC‑Exos <i>in</i> <i>vitro</i> and <i>in</i> <i>vivo</i> was assessed to explore the synergistic mechanisms underlying the effects of LIPUS. The <i>in</i> <i>vivo</i> results demonstrated that LIPUS increased the uptake of exosomes and prolonged the residence of exosomes in the wound area, thus enhancing angiogenesis and accelerating wound repair in diabetic mice. The <i>in</i> <i>vitro</i> results further confirmed that LIPUS enhanced the uptake efficiency of ADSC‑Exos by 10.93‑fold and significantly increased the proliferation, migration and tubular formation of HUVECs. Therefore, the present study indicates that LIPUS is a promising strategy to improve the therapeutic effects of ADSC‑Exos in diabetic wounds by promoting the cellular uptake of exosomes and enhancing angiogenesis.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":null,"pages":null},"PeriodicalIF":5.4,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10836517/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139424625","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-03-01Epub Date: 2024-02-01DOI: 10.3892/ijmm.2024.5353
Jing-Meng Hu, Li-Jie He, Peng-Bo Wang, Yan Yu, Ya-Ping Ye, Li Liang
Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that the EdU staining assay data shown in Figs. 4C and 5C and the western blotting data shown in Fig. 4E were strikingly similar to data appearing in different form in other research articles written by different authors at different research institutes that had either already been published, or were submitted for publication at around the same time. Owing to the fact that contentious data in the above article had already been submitted for publication elsewhere prior to its submission to International Journal of Molecular Medicine, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Molecular Medicine 48: 169, 2021; DOI: 10.3892/ijmm.2021.5002].
在这篇论文发表后,一位相关读者提请编辑注意,图 4C 和 5C 所示的 EdU 染色检测数据以及图 4E 所示的 Western 印迹数据与不同研究机构不同作者撰写的其他研究文章中以不同形式出现的数据惊人地相似,而这些文章要么已经发表,要么大约在同一时间提交发表。由于上述文章中有争议的数据在提交给《国际分子医学杂志》之前已经在其他地方发表,因此编辑决定从《国际分子医学杂志》撤回这篇论文。已要求作者就这些问题做出解释,但编辑部没有收到回复。对于给读者带来的不便,编辑深表歉意。[国际分子医学杂志 48:169, 2021; DOI: 10.3892/ijmm.2021.5002]。
{"title":"[Retracted] Antagonist targeting miR‑106b‑5p attenuates acute renal injury by regulating renal function, apoptosis and autophagy via the upregulation of TCF4.","authors":"Jing-Meng Hu, Li-Jie He, Peng-Bo Wang, Yan Yu, Ya-Ping Ye, Li Liang","doi":"10.3892/ijmm.2024.5353","DOIUrl":"10.3892/ijmm.2024.5353","url":null,"abstract":"<p><p>Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that the EdU staining assay data shown in Figs. 4C and 5C and the western blotting data shown in Fig. 4E were strikingly similar to data appearing in different form in other research articles written by different authors at different research institutes that had either already been published, or were submitted for publication at around the same time. Owing to the fact that contentious data in the above article had already been submitted for publication elsewhere prior to its submission to <i>International Journal of Molecular Medicine</i>, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Molecular Medicine 48: 169, 2021; DOI: 10.3892/ijmm.2021.5002].</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":null,"pages":null},"PeriodicalIF":5.4,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10852009/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139650750","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-03-01Epub Date: 2024-01-12DOI: 10.3892/ijmm.2024.5345
Hua Yan, Bing-Mei Sun, Yu-Ying Zhang, Yu-Juan Li, Cheng-Xiang Huang, Fu-Zhong Feng, Cui Li
Following the publication of this article, a concerned reader drew to the Editor's attention that, in Fig. 9C on p. 2478 showing the results of Transwell invasion assay experiments, unexpected areas of similarity were identified in terms of the cellular patterns revealed both within the data panels for the six different experiments portrayed in this figure, and comparing among them. After having conducted an internal investigation, the Editor of International Journal of Molecular Medicine has reached the conclusion that the overlapping sections of data shown in this figure were unlikely to have arisen by coincidence. Therefore, on the grounds of a lack of confidence in the integrity of these data, the Editor has decided that the article should be retracted from the publication. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused, and thanks the interested reader for drawing this matter to our attention. [International Journal of Molecular Medicine 42: 2469‑2480, 2018; DOI: 10.3892/ijmm.2018.3853].
在这篇文章发表后,一位相关读者提请编辑注意,在第 2478 页图 9C 显示的 Transwell 侵袭实验结果中,无论是在图中描绘的六个不同实验的数据板中,还是在它们之间的比较中,都发现了意想不到的细胞模式相似区域。经过内部调查,《国际分子医学杂志》编辑得出结论:本图中显示的数据重叠部分不太可能是巧合。因此,由于对这些数据的完整性缺乏信心,编辑决定从刊物上撤下这篇文章。作者被要求解释这些问题,但编辑部没有收到答复。对于给读者带来的不便,编辑深表歉意,并感谢感兴趣的读者提请我们注意此事。[International Journal of Molecular Medicine 42: 2469-2480, 2018; DOI: 10.3892/ijmm.2018.3853]。
{"title":"[Retracted] Upregulation of miR‑183‑5p is responsible for the promotion of apoptosis and inhibition of the epithelial‑mesenchymal transition, proliferation, invasion and migration of human endometrial cancer cells by downregulating Ezrin.","authors":"Hua Yan, Bing-Mei Sun, Yu-Ying Zhang, Yu-Juan Li, Cheng-Xiang Huang, Fu-Zhong Feng, Cui Li","doi":"10.3892/ijmm.2024.5345","DOIUrl":"10.3892/ijmm.2024.5345","url":null,"abstract":"<p><p>Following the publication of this article, a concerned reader drew to the Editor's attention that, in Fig. 9C on p. 2478 showing the results of Transwell invasion assay experiments, unexpected areas of similarity were identified in terms of the cellular patterns revealed both within the data panels for the six different experiments portrayed in this figure, and comparing among them. After having conducted an internal investigation, the Editor of <i>International Journal of Molecular Medicine</i> has reached the conclusion that the overlapping sections of data shown in this figure were unlikely to have arisen by coincidence. Therefore, on the grounds of a lack of confidence in the integrity of these data, the Editor has decided that the article should be retracted from the publication. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused, and thanks the interested reader for drawing this matter to our attention. [International Journal of Molecular Medicine 42: 2469‑2480, 2018; DOI: 10.3892/ijmm.2018.3853].</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":null,"pages":null},"PeriodicalIF":5.4,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10836491/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139424624","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}