{"title":"New insights into the role of ubiquitination in angiogenesis (Review).","authors":"Tao Chen, Keyu Wang, Ziqiang Sun","doi":"10.3892/ijmm.2024.5473","DOIUrl":"https://doi.org/10.3892/ijmm.2024.5473","url":null,"abstract":"<p><p>Angiogenesis is a dynamic and complex mechanism for generating new blood vessels from existing ones. Angiogenesis occurs through all life stages and involves several physiological processes. It has an important physiological and pathological role including in cancer, wound healing and inflammation. The emerging role of ubiquitination in regulating angiogenesis highlights the importance of studying this pathway in an angiogenic setting. In angiogenic events, imbalances between pro‑ and anti‑angiogenic factors, induction of hypoxic signaling and stimulation of angiogenic signaling pathways play a central role. This review provides a comprehensive overview of the role of ubiquitination in angiogenesis. This includes angiogenic factors [VEGF, platelet‑derived growth factor, (basic) fibroblast growth factor and angiopoietin], vascular cells (pericytes, endothelial cells, vascular smooth muscle cells) and extracellular matrix and cell adhesion molecules, all of which have important roles in angiogenesis, hypoxic signaling (hypoxia‑inducible factor), which induces angiogenesis, and important vascular signaling pathways (Wnt and Notch). In addition, the molecular biological basis of angiogenesis is discussed and the potential therapeutic value of ubiquitination in angiogenesis‑related diseases is highlighted.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"55 2","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142864218","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":"Adrenic acid: A promising biomarker and therapeutic target (Review).","authors":"Ze Wang, Haoyang Gao, Xiaotong Ma, Danlin Zhu, Linlin Zhao, Weihua Xiao","doi":"10.3892/ijmm.2024.5461","DOIUrl":"10.3892/ijmm.2024.5461","url":null,"abstract":"<p><p>Adrenic acid is a 22‑carbon unsaturated fatty acid that is widely present in the adrenal gland, liver, brain, kidney and vascular system that plays a regulatory role in various pathophysiological processes, such as inflammatory reactions, lipid metabolism, oxidative stress, vascular function, and cell death. Adrenic acid is a potential biomarker for various ailments, including metabolic, neurodegenerative and cardiovascular diseases and cancer. In addition, adrenic acid is influenced by the pharmacological properties of several natural products, such as astragaloside IV, evodiamine, quercetin, kaempferol, Berberine‑baicalin and prebiotics, so it is a promising new target for clinical treatment and drug development. However, the molecular mechanisms by which adrenic acid exerts are unclear. The present study systematically reviewed the biosynthesis and metabolism of adrenic acid, focusing on intrinsic mechanisms that influence the progression of metabolic, cardiovascular and neurological disease. These mechanisms regulate several key processes, including immuno‑inflammatory response, oxidative stress, vascular function and cell death. In addition, the present study explored the potential clinical translational value of adrenic acid as a biomarker and therapeutic target. To the best of our knowledge, the present study is first systematic summary of the mechanisms of action of adrenic acid across a range of diseases. The present study provides understanding of the wide range of metabolic activities of adrenic acid and a basis for further exploring the pathogenesis and therapeutic targets of various diseases.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"55 2","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11611323/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142686926","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 DNA methylation transferase in urinary system diseases: From basic to clinical perspectives (Review).","authors":"Yipin Yang, Yafen Wang, Xiufang Fan, Xinwei Xu, Huijuan Wang, Xinyi Wang, Taiyu Shi, Jialu Tang, Yanmeng Guan, Song Li, Aimei Wang","doi":"10.3892/ijmm.2024.5460","DOIUrl":"10.3892/ijmm.2024.5460","url":null,"abstract":"<p><p>DNA methylation is one of the earliest discovered and most extensively studied epigenetic regulatory mechanisms. Broadly, DNA methylation refers to the transfer of a methyl group on S‑adenosine‑L‑methionine (SAM) to the C5 site of cytosine, a reaction catalysed by DNA methyltransferase (DNMT). This process can either up‑ or down‑regulate gene expression due to gene promoter methylation, leading to the occurrence of certain diseases. Urinary system diseases, known for their high prevalence and complex pathogenesis, significantly affect the lives and health of patients. Urological tumours, in particular, represent a non‑negligible disease burden worldwide. With the development of epigenetics, an increasing number of studies have demonstrated that DNMT plays an important role in urinary system disease. The present review aims to explore the relationship between DNMT and urinary system diseases and the potential of DNMT in the clinical management of these diseases.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"55 2","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11611324/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142686929","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}
Lumiao Zhang, Mengjia Jing, Qianben Song, Yiming Ouyang, Yingzhi Pang, Xilin Ye, Yu Fu, Wei Yan
{"title":"Role of the m<sup>6</sup>A demethylase ALKBH5 in gastrointestinal tract cancer (Review).","authors":"Lumiao Zhang, Mengjia Jing, Qianben Song, Yiming Ouyang, Yingzhi Pang, Xilin Ye, Yu Fu, Wei Yan","doi":"10.3892/ijmm.2024.5463","DOIUrl":"10.3892/ijmm.2024.5463","url":null,"abstract":"<p><p>N6‑methyladenosine (m<sup>6</sup>A) is one of the most universal, abundant and conserved types of internal post‑transcriptional modifications in eukaryotic RNA, and is involved in nuclear RNA export, RNA splicing, mRNA stability, gene expression, microRNA biogenesis and long non‑coding RNA metabolism. AlkB homologue 5 (ALKBH5) acts as a m6A demethylase to regulate a wide variety of biological processes closely associated with tumour progression, tumour metastasis, tumour immunity and tumour drug resistance. ALKBH5 serves a crucial role in human digestive system tumours, mainly through post‑transcriptional regulation of m<sup>6</sup>A modification. The present review discusses progress in the study of the m6A demethylase ALKBH5 in gastrointestinal tract cancer, summarizes the potential molecular mechanisms of ALKBH5 dysregulation in gastrointestinal tract cancer, and discusses the significance of ALKBH5‑targeted therapy, which may provide novel ideas for future clinical prognosis prediction, biomarker identification and precise treatment.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"55 2","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11637504/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142750711","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}
Shengnan Sun, Shurong Yang, Ying Cheng, Ting Fang, Jingru Qu, Lei Tian, Man Zhang, Shi Wu, Bei Sun, Liming Chen
{"title":"Jinlida granules alleviate podocyte apoptosis and mitochondrial dysfunction via the AMPK/PGC‑1α pathway in diabetic nephropathy.","authors":"Shengnan Sun, Shurong Yang, Ying Cheng, Ting Fang, Jingru Qu, Lei Tian, Man Zhang, Shi Wu, Bei Sun, Liming Chen","doi":"10.3892/ijmm.2024.5467","DOIUrl":"10.3892/ijmm.2024.5467","url":null,"abstract":"<p><p>Traditional Chinese Medicine (TCM) has demonstrated promising efficacy in managing and preventing the early‑stage diabetic nephropathy (DN). Although the exact mechanisms remain elusive, clinical evidence has suggested that Jinlida granules (JLD) are beneficial in improving renal function among patients with DN. The present study aimed to elucidate the effect of JLD on DN and the underlying molecular mechanism. Therefore, podocyte apoptosis was evaluated using flow cytometry and TUNEL staining, while mitochondrial morphology and function were assessed using transmission electron microscopy, MitoTracker, JC‑1 and reactive oxygen species staining. RNA sequencing analysis was performed to elucidate the mechanism underlying the effect of JLD on DN. Additionally, to investigate the role of peroxisome proliferator‑activated receptor‑γ co‑activator‑1α (PGC‑1α) in mitigating JLD‑induced mitochondrial dysfunction and podocyte apoptosis, MPC5 cells were transfected with the corresponding small interfering RNA constructs. The results showed that JLD effectively improved renal function and mitigated podocyte injury, as well as ameliorated mitochondrial dysfunction and inhibited apoptosis in db/db mice. <i>In vitro</i> experiments further revealed that JLD exerted a protective effect via inhibiting mitochondrial fission and apoptosis in high glucose‑treated podocytes. Furthermore, JLD enhanced the phosphorylation of adenosine monophosphate‑activated protein kinase (AMPK), thus promoting the expression of PGC‑1α, eventually improving apoptosis and mitochondrial homeostasis. Overall, the current study revealed that JLD could improve mitochondrial homeostasis and reduce cell apoptosis in podocytes via activating the AMPK/PGC‑1α pathway, thus providing a theoretical foundation for the clinical management of DN.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"55 2","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142818179","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}
Xinting Pan, Qingyun Zhu, Yunbo Sun, Liandi Li, Yunpeng Zhu, Zhihui Zhao, Jianxin Zuo, Wei Fang, Kun Li
{"title":"[Retracted] PLGA/poloxamer nanoparticles loaded with EPAS1 siRNA for the treatment of pancreatic cancer <i>in vitro</i> and <i>in vivo</i>.","authors":"Xinting Pan, Qingyun Zhu, Yunbo Sun, Liandi Li, Yunpeng Zhu, Zhihui Zhao, Jianxin Zuo, Wei Fang, Kun Li","doi":"10.3892/ijmm.2024.5459","DOIUrl":"10.3892/ijmm.2024.5459","url":null,"abstract":"<p><p>Following the publication of this article, a concerned reader drew to the Editor's attention that, in the tumor tissue images shown in Fig. 5A and B on p. 1001, there were two pairs of overlapping data panels, such that data which were intended to show the results from differently performed experiments appeared to have been derived from the same original sources. Subsequently, after having conducted a separate investigation in the Editorial Office, it came to light that there were also matching data panels intending to show the results from different experiments in the flow cytometric plots shown in Fig. 2; moreover, there appeared to be potential issues with the presentation of some of the western blots in Fig. 3. Although the possibility of a corrigendum was considered, upon reflection, the Editor of <i>International Journal of Molecular Medicine</i> has decided that, owing to the number of problems that were identified with the data in the published paper, the article should be retracted from the publication on account of data mishandling issues and an overall lack of confidence in the presented data. 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 initially drawing this matter to our attention.[International Journal of Molecular Medicine 35: 995‑1002, 2015; DOI: 10.3892/ijmm.2015.2096].</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"55 2","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11611322/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142686923","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}
Barbara Quaresima, Stefania Scicchitano, Maria Concetta Faniello, Maria Mesuraca
{"title":"Role of solute carrier transporters in ovarian cancer (Review).","authors":"Barbara Quaresima, Stefania Scicchitano, Maria Concetta Faniello, Maria Mesuraca","doi":"10.3892/ijmm.2024.5465","DOIUrl":"10.3892/ijmm.2024.5465","url":null,"abstract":"<p><p>Solute carrier (SLC) transporters are involved in various biological processes associated with metabolic reprogramming and cancer, supporting the increased requirement of nutrients and energy. Over the past decade, there have been significant advancements in understanding the expression and function of SLCs in ovarian cancer (OC). This gynecological condition has a high mortality rate and limited treatment options; thus, early diagnosis remains a target clinically. OC exhibits complexity and heterogeneity, resulting in different clinical characteristics, resistance to chemotherapy drugs and poor prognosis. Additionally, SLCs have a different expression pattern between healthy and tumor tissue, and consequently, their inhibition or activation could modify signaling pathways involved in the tumor growth process, such as cell proliferation, apoptosis and drug accumulation. The present review aims to consolidate current data to provide a comprehensive understanding of the potential importance of SLCs in OC. Additionally, it seeks to offer guidance for further research on utilizing SLCs as prognostic biomarkers and therapeutic targets.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"55 2","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11637498/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142750675","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}
Cheng Wang, Lu Wang, Ziling Wang, Zesong Yang, Kunhang Du, Jiaqi Song, Jiying Hou, Yaping Wang
{"title":"Study on the <i>in vitro</i> changes of human bone marrow‑related mesenchymal stem cells.","authors":"Cheng Wang, Lu Wang, Ziling Wang, Zesong Yang, Kunhang Du, Jiaqi Song, Jiying Hou, Yaping Wang","doi":"10.3892/ijmm.2024.5464","DOIUrl":"10.3892/ijmm.2024.5464","url":null,"abstract":"<p><p>Bone marrow mesenchymal stem cells (MSCs) serve a pivotal role in the hematopoietic niche. The present study collected bone marrow samples from individuals across various age groups to investigate the biological characteristics of MSCs. By modifying the bone marrow microenvironment through co‑culture techniques, changes in the stemness of MSCs were examined. An <i>in vitro</i> hematopoietic co‑culture system was established to simulate the impact of MSCs on hematopoietic stem cells. The results demonstrated that the mode of cell‑to‑cell contact among stem cells is more influential in shaping bone marrow function compared with the effects of aging on these stem cells. Transcriptomic analysis revealed that MSCs serve as essential mediators, with their growth variations being both a consequence and a cause of changes in the bone marrow microenvironment. Furthermore, the decline in hematopoietic function observed in the elderly is a manifestation of this phenomenon. Data from the present study suggest that targeting MSCs is essential for enhancing bone marrow function and improving the outcomes of bone marrow transplantation.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"55 2","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11637496/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142750715","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}
Dan Liu, Chao Liu, Fei Deng, Fumin Ouyang, Rongxin Qin, Zhaoxia Zhai, Yan Wang, Yu Zhang, Mengling Liao, Xichun Pan, Yasi Huang, Yanyan Cen, Xiaoli Li, Hong Zhou
{"title":"Artesunate protects against a mouse model of cerulein and lipopolysaccharide‑induced acute pancreatitis by inhibiting TLR4‑dependent autophagy.","authors":"Dan Liu, Chao Liu, Fei Deng, Fumin Ouyang, Rongxin Qin, Zhaoxia Zhai, Yan Wang, Yu Zhang, Mengling Liao, Xichun Pan, Yasi Huang, Yanyan Cen, Xiaoli Li, Hong Zhou","doi":"10.3892/ijmm.2024.5466","DOIUrl":"10.3892/ijmm.2024.5466","url":null,"abstract":"<p><p>Severe acute pancreatitis (SAP) is a severe clinical condition associated with high rates of morbidity and mortality. Multiple organ dysfunction syndrome that follows systemic inflammatory response syndrome is the leading cause of SAP‑related death. Since the inflammatory mechanism of SAP remains unclear, there is currently a lack of effective drugs available for its treatment. Therefore, it is important to study effective therapeutic drugs and their molecular mechanisms based on studying the inflammatory mechanism of SAP. In the present study, <i>in vivo</i>, a mouse model of AP induced by cerulein (CR) combined with lipopolysaccharide (LPS) was established to clarify the therapeutic effect of artesunate (AS) in AP mice by observing the gross morphological changes of the pancreas and surrounding tissues, calculating the pancreatic coefficient, and observing the histopathology of the pancreas. The serum amylase activity in AP mice was detected by iodine colorimetry and the superoxide dismutase activity in the pancreas was detected by WST‑1 assay. The levels of proinflammatory cytokines in the serum, the supernatant of pancreatic tissue homogenates and the peritoneal lavage fluid were detected by ELISA assay. The total number of peritoneal macrophages was assessed using the cellular automatic counter, and the expression of proteins related to autophagy, and the TLR4 pathway was detected by immunohistochemistry and western blotting. <i>In vitro</i>, the effect of trypsin (TP) combined with LPS was observed by detecting the release of proinflammatory cytokine levels from macrophages by ELISA assay, and detecting the expression of proteins related to autophagy and the TLR4 pathway by immunofluorescence and western blotting. The present study revealed that AS reduced pancreatic histopathological damage, decreased pancreatic TP and serum amylase activities, increased superoxide dismutase activity, and inhibited pro‑inflammatory cytokine levels in a mouse model of AP induced by cerulein combined with lipopolysaccharide. <i>In vitro</i>, TP combined with LPS was found to synergistically induce pro‑inflammatory cytokine release from mouse macrophages and RAW264.7 cells, while AS could inhibit cytokine release. Furthermore, CR combined with LPS synergistically increased amylase activity in acinar cells, whereas AS decreased amylase activity. Autophagy serves an important role in the release of pro‑inflammatory cytokines. In the present study, it was revealed that the autophagy inhibitor LY294002 suppressed the release of pro‑inflammatory cytokines from macrophages treated with TP combined with LPS, and pro‑inflammatory cytokine release was not further reduced by AS combined with LY294002. Furthermore, AS not only inhibited the expression of important molecules in the Toll‑like receptor 4 (TLR4) signaling pathway, but also inhibited autophagy proteins and reduced the number of autolysosomes in mice with AP and in macrophages. In conclusion, these resu","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"55 2","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11637502/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142785322","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":"[Corrigendum] Abnormal expression of SIRTs in psoriasis: Decreased expression of SIRT 1‑5 and increased expression of SIRT 6 and 7.","authors":"Xiaojing Fan, Kexiang Yan, Qinqin Meng, Rui Sun, Xinrong Yang, Dingfen Yuan, Fulun Li, Hui Deng","doi":"10.3892/ijmm.2024.5472","DOIUrl":"https://doi.org/10.3892/ijmm.2024.5472","url":null,"abstract":"<p><p>Following the publication of the above article, the authors contacted the Editorial Office to explain that three pairs of the western blots featured in Fig. 4 on p. 165 had inadvertently been duplicated in this figure. Essentially, it appeared to the authors that the blots in Fig. 4A for SIRT5 were identical to those in Fig. 4C for SIRT6 (P2 versus C2); the blots in Fig. 4B for SIRT4 were identical to those in the same figure part for SIRT5; and the blots in Fig. 4C for SIRT6 (P3 versus C3) were identical to those in Fig. 4C for SIRT7 (P1 versus C1). The authors were able to re‑examine their original data, and identified the data that should have rightfully been included in this figure. The revised version of Fig. 4, now incorporating the correct data for SIRT6 (P2 versus C2) in Fig. 4C, SIRT5 in Fig. 4B, and SIRT7 (P1 versus C1) in Fig. 4C, 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 44: 157‑171, 2019; DOI: 10.3892/ijmm.2019.4173].</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"55 2","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142864205","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}