International journal of molecular medicine最新文献

{"title":"[Retracted] Ginsenoside Rg3 ameliorates acute pancreatitis by activating the NRF2/HO‑1‑mediated ferroptosis pathway.","authors":"Yuqiang Shan, Jiaotao Li, Akao Zhu, Wencheng Kong, Rongchao Ying, Weiming Zhu","doi":"10.3892/ijmm.2024.5449","DOIUrl":"10.3892/ijmm.2024.5449","url":null,"abstract":"<p><p>Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that certain of the flow cytometric data shown in Fig. 1D, DCFH‑DA‑stained cellular data in Fig. 2A, and western blotting data in Figs. 2G and 5B were strikingly similar to data that had either already appeared in previously published articles written by different authors at different research institutes (one of which has since been retracted), or were featured in an article that was submitted for publication to a different journal at around the same time. Owing to the fact that the contentious data in the above article had already been published 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 50: 89, 2022; DOI: 10.3892/ijmm.2022.5144].</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"55 1","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11554378/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142604467","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}

{"title":"Enocyanin promotes osteogenesis and bone regeneration by inhibiting MMP9.","authors":"Wei Mao, Yinfeng Zheng, Wencong Zhang, Jinrong Yin, Zhiyi Liu, Peiliang He, Guodong Hou, Guowei Huang, Huan Chen, Junyan Lin, Jiake Xu, Aiguo Li, Shengnan Qin","doi":"10.3892/ijmm.2024.5450","DOIUrl":"10.3892/ijmm.2024.5450","url":null,"abstract":"<p><p>Enocyanin (ENO), an anthocyanin extracted from grapes, has been shown to exert inhibitory effects on acid phosphatase and inflammation; however, its role in osteogenesis and bone formation is currently unknown. The present study aimed to investigate the effects of ENO on osteogenesis <i>in vitro</i> and bone formation <i>in vivo</i>, and to explore the rudimentary mechanisms. KusaO cells were employed to evaluate the osteogenic role of ENO <i>in vitro</i> by Alizarin red S staining, ALP staining, quantitative PCR and western blotting, and an <i>in vivo</i> analysis of the therapeutic effects of ENO on a femoral fracture model was performed using stereo microscope, micro‑CT and histological staining. To further investigate the underlying mechanisms, mRNA sequencing was employed to investigate the changes in gene expression and the downstream pathways after ENO treatment. The results showed that ENO could promote the osteogenic differentiation of KusaO cells <i>in vitro</i> and bone fracture regeneration <i>in vivo</i>. Mechanistically, ENO was highly related to bone formation, including the 'Wnt signalling pathway', 'bone development' and 'bone mineralization'. In addition, matrix metalloproteinase 9 (MMP9) was identified as one of the targets of ENO in its promotional role in osteogenesis. In conclusion, ENO may represent a therapeutic candidate for bone regeneration in bone fractures by regulating osteogenesis and bone formation via MMP9.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"55 1","pages":""},"PeriodicalIF":8.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11554379/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142604488","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}

{"title":"Role of Sam68 in different types of cancer (Review).","authors":"Carlos Jiménez-Cortegana, Flora Sánchez-Jiménez, Luis De La Cruz-Merino, Víctor Sánchez-Margalet","doi":"10.3892/ijmm.2024.5444","DOIUrl":"10.3892/ijmm.2024.5444","url":null,"abstract":"<p><p>Src‑associated in mitosis 68 kDa protein (Sam68) is a protein encoded by the heteronuclear ribonucleoprotein particle K homology (KH) single domain‑containing, RNA‑binding, signal transduction‑associated protein 1 (known as <i>KHDRBS1</i>) gene in humans. This protein contains binding sites for critical components in a variety of cellular processes, including the regulation of gene expression, RNA processing and cell signaling. Thus, Sam68 may play a role in a variety of diseases, including cancer. Sam68 has been widely demonstrated to participate in tumor cell proliferation, progression and metastasis to be involved in the regulation of cancer stem cell self‑renewal. Based on the body of evidence available, Sam68 emerges as a promising target for this disease. The objectives of the present included summarizing the role of Sam68 in cancer murine models and cancer patients, unraveling the molecular mechanisms underlying its oncogenic potential and discussing the effectiveness of antitumor agents in reducing the malignant effects of Sam68 during tumorigenesis.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"55 1","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11537268/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142499909","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}

{"title":"Circular RNAs in coronary heart disease: From molecular mechanism to promising clinical application (Review).","authors":"Zengguang Fan, Xingxing Yuan, Ye Yuan","doi":"10.3892/ijmm.2024.5452","DOIUrl":"10.3892/ijmm.2024.5452","url":null,"abstract":"<p><p>Coronary heart disease (CHD) remains a leading cause of morbidity and mortality worldwide, posing a substantial public health burden. Despite advancements in treatment, the complex etiology of CHD necessitates ongoing exploration of novel diagnostic markers and therapeutic targets. Circular RNAs (circRNAs), a distinct class of non‑coding RNAs with a covalently closed loop structure, have emerged as significant regulators in various diseases, including CHD. Their high stability, tissue‑specific expression and evolutionary conservation underscore their potential as biomarkers and therapeutic agents in CHD. This review discusses the current knowledge on circRNAs in the context of CHD and explores the molecular mechanisms by which circRNAs influence the pathophysiology of CHD, including cardiomyocyte death, endothelial injury, vascular dysfunction and inflammation. It also summarizes the emerging evidence highlighting the differential expression of circRNAs in patients with CHD and their potential utilities as non‑invasive diagnostic and prognostic biomarkers and therapeutic targets for this disease.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"55 1","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11573316/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142604474","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}

{"title":"[Retracted] Adipose extracellular matrix promotes skin wound healing by inducing the differentiation of adipose‑derived stem cells into fibroblasts.","authors":"Zhi-Qiang Zhou, Yi Chen, Mi Chai, Ran Tao, Yong-Hong Lei, Yi-Qing Jia, Jun Shu, Jing Ren, Guo Li, Wen-Xin Wei, Yu-Di Han, Yan Han","doi":"10.3892/ijmm.2024.5430","DOIUrl":"10.3892/ijmm.2024.5430","url":null,"abstract":"<p><p>Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that certain of the immunohistochemical images shown in Fig. 2B and C on p. 896 were strikingly similar to data appearing in different form in other articles written by different authors at different research institutes that had already been published before this paper was received at <i>International Journal of Molecular Medicine</i> (several of which have been retracted). Moreover, the flow-cytometric data shown in Fig. 2A appeared to be potentially anomalous. In view of the fact that the abovementioned data had already apparently been published prior to the submission of this paper to <i>International Journal of Molecular Medicine</i>, the Editor has decided that the article 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 43: 890-900, 2019; DOI: 10.3892/ijmm.2018.4006].</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"54 6","pages":""},"PeriodicalIF":5.7,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11448557/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142380803","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}

{"title":"Glycolysis modulation: New therapeutic strategies to improve pulmonary hypertension (Review).","authors":"Meihong Chen, Hui Li, Yun Li, Yangui Luo, Yuan He, Xiaorong Shui, Wei Lei","doi":"10.3892/ijmm.2024.5439","DOIUrl":"10.3892/ijmm.2024.5439","url":null,"abstract":"<p><p>Pulmonary hypertension (PH) is a progressive life‑threatening cardiopulmonary vascular disease involving various pathological mechanisms, including hypoxia, cellular metabolism, inflammation, abnormal proliferation and apoptosis. Specifically, metabolism has attracted the most attention. Glucose metabolism is essential to maintain the cardiopulmonary vascular function. However, once exposed to a noxious stimulus, intracellular glucose metabolism changes or switches to an alternative pathway more suitable for adaptation, which is known as metabolic reprogramming. By promoting the switch from oxidative phosphorylation to glycolysis, cellular metabolic reprogramming plays an important role in PH development. Suppression of glucose oxidation and secondary upregulation of glycolysis are responsible for various features of PH, including the proliferation and apoptosis resistance of pulmonary artery endothelial and smooth muscle cells. In the present review, the roles and importance of the glucose metabolism shift were discussed to aid in the development of new treatment approaches for PH.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"54 6","pages":""},"PeriodicalIF":5.7,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11518579/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142464654","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}

{"title":"New insight for SS‑31 in treating diabetic cardiomyopathy: Activation of mitoGPX4 and alleviation of mitochondria‑dependent ferroptosis.","authors":"Lie Xiong, Huilin Hu, Fuxiang Zhu, Hanqiang Shi, Xiaoliang Fan, Sunfeng Pan, Feiye Zhu, Junyong Zhang, Zhongwei Yu, Yanbo Shi","doi":"10.3892/ijmm.2024.5436","DOIUrl":"10.3892/ijmm.2024.5436","url":null,"abstract":"<p><p>SS‑31 is a mitochondria‑targeting antioxidant that exhibits promising therapeutic potential for various diseases; however, its protective effect on diabetic cardiomyopathy (DCM) remains to be elucidated. At present, SS‑31 is considered not only to mitigate cardiolipin oxidative damage, but also to alleviate ferroptosis. The present study aimed to explore SS‑31 as a potential therapeutic strategy for improving DCM by alleviating mitochondria‑dependent ferroptosis. In vitro, H9C2 cells were exposed to 35 mM glucose for 24 h to induce high glucose damage, then were simultaneously treated with 10, 20 or 50 µM SS‑31. In addition, in vivo studies were conducted on diabeticC57BL/6J mice, which were induced to develop DCM over 4 weeks, followed by intraperitoneal injections with 2.5 mg/kg/day SS‑31 for a further 4 weeks. The elevation of serum lactate dehydrogenase and creatine kinase isoenzymes, the reduction of fractional shortening and ejection fraction, the rupture of myocardial fibers and the deposition of collagen indicated the establishment of the DCM mouse model. The results of the present study indicated that SS‑31 effectively alleviated these pathological changes and exhibited significant efficacy in ameliorating mitochondrial dysfunction, such as by promoting adenosine triphosphate generation, improving mitochondrial membrane potential and restoring the mitochondrial ultrastructure. Further experiments suggested that activation of the mitochondrial glutathione (mitoGSH)/mitochondrial glutathione peroxidase 4 (mitoGPX4) pathway and the elimination of mitochondrial ferrous ions may constitute the mechanisms by which SS‑31 treats DCM. Therefore, the present study revealed that mitochondria‑dependent ferroptosis could serve as a pathogenic mechanism of DCM and highlighted that the cardioprotective effects of SS‑31 against DCM involves activation of the mitoGSH/mitoGPX4 pathway. Due to the safety profile and cardiac protective effects of SS‑31, SS‑31 was considered a promising strategy for treating DCM.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"54 6","pages":""},"PeriodicalIF":5.7,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11517773/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142371807","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}

{"title":"Protein biomarkers in assessing kidney quality before transplantation‑current status and future perspectives (Review).","authors":"Maksymilian Baryła, Michał Skrzycki, Roman Danielewicz, Maciej Kosieradzki, Marta Struga","doi":"10.3892/ijmm.2024.5431","DOIUrl":"10.3892/ijmm.2024.5431","url":null,"abstract":"&lt;p&gt;&lt;p&gt;To meet the demand for kidney transplants (KTx), organs are frequently retrieved not only from standard criteria donors (SCD; a donor who is aged &lt;50 years and suffered brain death from any number of causes, such as traumatic injuries or a stroke) but also from expanded criteria donors (any donor aged &gt;60 years or donors aged &gt;50 years with two of the following: A history of high blood pressure, a creatinine serum level ≥1.5 mg/dl or death resulting from a stroke). This comes at the cost of a higher risk of primary non‑function (the permanent hyperkalemia, hyperuremia and fluid overload that result in the need for continuous dialysis after KTx), delayed graft function (the need for dialysis session at least once during the first week after KTx), earlier graft loss and urinary complications (vesico‑ureteral reflux, obstruction of the vesico‑ureteral anastomosis, urine leakage). At present, there are no commercially available diagnostic tools for assessing kidney quality prior to KTx. Currently available predictive models based on clinical data, such as the Kidney Donor Profile Index, are insufficient. One promising option is the application of perfusion solutions for protein biomarkers of kidney quality and predictors of short‑ and long‑term outcomes. However, to date, protein markers that can be detected with ELISA, western blotting and cytotoxic assays have not been identified to be a beneficial predictors of kidney quality. These include lactate dehydrogenases, glutathione S‑transferases, fatty acid binding proteins, extracellular histones, IL‑18, neutrophil gelatinase‑associated lipocalin, MMPs and kidney injury molecule‑1. However, novel methods, including liquid chromatography‑mass spectrometry (LC‑MS) and microarrays, allow the analysis of all renal proteins suspended/dissolved in the acellular preservation solution used for kidney storage before KTx (including hypothermic machine perfusion as one of kidney storage methods) e.g. Belzer University of Wisconsin. Recent proteomic studies utilizing LC‑MS have identified complement pathway elements (C3, C1QB, C4BPA, C1S, C1R and C1RL), desmoplakin, blood coagulation pathway elements and immunoglobulin heavy variable 2‑26 to be novel predictors of kidney quality before transplantation. This was because they were found to correlate with estimated glomerular filtration rate at 3 and 12 months after kidney transplantation. However, further proteomic studies focusing on distinct markers obtained from hypothermic and normothermic machine perfusion are needed to confirm their predictive value and to improve kidney storage methods. Therefore, the present literature review from PubMed, Scopus, Embase and Web of Science was performed with the aims of summarizing the current knowledge on the most frequently studied single protein biomarkers. In addition, novel analytical methods and insights into organ injury during preservation were documented, where future directions in assessing organ quality befo","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"54 6","pages":""},"PeriodicalIF":5.7,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11448562/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142380804","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}

{"title":"From banked human cord blood to induced pluripotent stem cells: New opportunities and promise in induced pluripotent stem cell banking (Review).","authors":"Fatin Fazrina Roslan, Yuexin Yu, Ghee Chien Ooi, Khong Lek Then, Kong Yong Then, Soon-Keng Cheong, Zhikun Guo, Mohd Nor Azim Ab Patar, Jun Jie Tan","doi":"10.3892/ijmm.2024.5438","DOIUrl":"https://doi.org/10.3892/ijmm.2024.5438","url":null,"abstract":"<p><p>Umbilical cord blood (CB) is a valuable source of haematopoietic stem/progenitor cells (HSCs) and is known for the therapeutic use of these cells in treating blood disorders. However, challenges such as a high running cost and the increasing availability of treatment alternatives have made the effort to sustain CB banks difficult. This prompts the need to revisit the current CB banking initiatives to retain the relevance in this ever‑changing era parallel to the fast‑pacing development of cell‑based therapeutic technology. Cellular reprogramming has shown to have successfully converted adult somatic cells into human induced pluripotent stem cells (hiPSCs), which promise wider applications in regenerative medicine, personalized treatment and tissue engineering. CB is the youngest, primitive adult cell source that has not been affected by any prior, acquired disorders. Hence, using CB as a source of candidate cells for generating hiPSCs may be a new opportunity for banking, albeit with challenges. The present review summarizes the rise and fall of CB usage and banking for clinical therapy, the considerations in reprogramming CB into hiPSCs, the safety concerns regarding the use of hiPSC‑derived cells in clinical transplantation and the prospect of using CB‑derived hiPSCs.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"54 6","pages":""},"PeriodicalIF":5.7,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142464653","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}

{"title":"Advances in the understanding of the role and mechanism of action of PFKFB3‑mediated glycolysis in liver fibrosis (Review).","authors":"Qian Liu, Jiajia Li, Xin Li, Li Zhang, Shun Yao, Yongfeng Wang, Biguang Tuo, Hai Jin","doi":"10.3892/ijmm.2024.5429","DOIUrl":"10.3892/ijmm.2024.5429","url":null,"abstract":"<p><p>Liver fibrosis is a pathophysiologic manifestation of chronic liver disease and a precursor to cirrhosis and hepatocellular carcinoma. Glycolysis provides intermediate metabolites as well as energy support for cell proliferation and phenotypic transformation in liver fibers. 6‑Phosphofructo‑2‑kinase/fructose‑2,6‑bisphosphatase 3 (PFKFB3) is a key activator of glycolysis and plays an important role in the process of glycolysis. The role of PFKFB3‑mediated glycolysis in myocardial fibrosis, renal fibrosis and pulmonary fibrosis has been demonstrated, and the role of PFKFB3 in the activation of hepatic stellate cells by aerobic glycolysis has been proven by relevant experiments. The present study reviews the research progress on the role and mechanism of action of PFKFB3‑mediated glycolysis in the progression of hepatic fibrosis to discuss the role of PFKFB3‑mediated glycolysis in hepatic fibrosis and to provide new ideas for research on PFKFB3 as a target for the treatment of hepatic fibrosis.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"54 6","pages":""},"PeriodicalIF":5.7,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11448561/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142286479","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}