International journal of molecular medicine最新文献

{"title":"Giant <i>Centella asiatica</i>, a novel cultivar rich in madecassoside and asiaticoside, suppresses α‑melanocyte‑stimulating hormone‑induced melanogenesis through MC1R binding.","authors":"Jiwon Seo, Chanhyeok Jeong, Seung Man Oh, Sung-Young Lee, Han Woong Park, Dae Bang Seo, Dae Sung Yoo, Woo-Jin Sim, Tae-Gyu Lim, Jung Han Yoon Park, Chang Hyung Lee, Ki Won Lee","doi":"10.3892/ijmm.2024.5454","DOIUrl":"10.3892/ijmm.2024.5454","url":null,"abstract":"<p><p>The present study investigated the anti‑melanogenesis effects of Giant <i>Centella asiatica</i> (GCA), a new cultivator of <i>Centella asiatica</i> (CA) cataloged by the Korea Forest Service in 2022, and compared its efficacy with that of traditional CA. GCA has a high yield per unit area and enhanced antioxidant properties. The anti‑melanogenic effects of GCA were investigated using B16F10 melanoma cells and a 3D human skin‑equivalent model. Key molecular mechanisms were elucidated through western blotting, cAMP assays and molecular docking studies. Focus was addressed on the effect of GCA on skin whitening by comparing the ability of a GCA extract to inhibit melanin production in B16F10 melanoma cells and a 3D human skin‑equivalent model to that of CA. The results showed that the GCA extracts more effectively reduced melanin production, which was attributed to their higher content of two active components, madecassoside and asiaticoside. Further investigation revealed that GCA primarily inhibited melanogenesis through the PKA‑cAMP response element‑binding (CREB)‑microphthalmia‑associated transcription factor (MITF) axis, a key regulatory pathway in melanin synthesis. Notably, the present study, to the best of our knowledge, is the first to demonstrate that madecassoside and asiaticoside, the two principal compounds in GCA, directly bound to MC1R, which contributed to the significant skin‑whitening effects. Moreover, GCA reduced melanin production in a 3D human skin‑equivalent model, showing efficacy within a complex skin environment. These results demonstrated the superior effectiveness of GCA to that of CA for skin anti‑melanogenesis, indicating its potential as a promising natural material for targeting pigmentation disorders.</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/PMC11573313/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142604491","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":"TP53 mutations in cancer: Molecular features and therapeutic opportunities (Review).","authors":"Maria Lina Tornesello","doi":"10.3892/ijmm.2024.5448","DOIUrl":"10.3892/ijmm.2024.5448","url":null,"abstract":"<p><p>The tumour suppressor factor p53 plays an essential role in regulating numerous cellular processes, including the cell cycle, DNA repair, apoptosis, autophagy, cell metabolism and immune response. TP53 is the most commonly mutated gene in human cancers. These mutations are primarily non‑synonymous changes that produce mutant p53 proteins characterized by loss of function, a dominant negative effect on p53 tetramerisation and gain of function (GOF). GOF mutations not only disrupt the tumour‑suppressive activities of p53 but also endow the mutant proteins with new oncogenic properties. Recent studies analysing different pathogenic features of mutant p53 in cancer‑derived cell lines have demonstrated that restoring wild‑type p53, rather than removing GOF mutations, reduces cancer cell growth. These findings suggest that therapeutic strategies for reactivating wild‑type p53 function in cancer cells may bring a greater benefit than approaches halting mutant p53. This approach could involve the use of small molecules, gene therapy and other methods to re‑establish wild‑type p53 activity. This review describes the complexity of the biological activities of different p53 mutants and summarizes the current therapeutic approaches to restore p53 function.</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/PMC11554381/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142499910","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":"Interplay between lncRNAs and the PI3K/AKT signaling pathway in the progression of digestive system neoplasms (Review).","authors":"Xiaoyu Zhang, Lei Shi, Mengzhen Xing, Chunjing Li, Fengjun Ma, Yuning Ma, Yuxia Ma","doi":"10.3892/ijmm.2024.5456","DOIUrl":"10.3892/ijmm.2024.5456","url":null,"abstract":"<p><p>Long non‑coding RNA (lncRNA) is a class of non‑coding RNA molecules located in the cytoplasm or nucleus, which can regulate chromosome structure and function by interacting with DNA, RNA, proteins and other molecules; binding to mRNA bases in a complementary manner, affecting the splicing, stabilization, translation and degradation of mRNA; acting as competing endogenous RNA competitively binds to microRNAs to regulate gene expression and participate in the regulation of various vital activities of the body. The PI3K/AKT signalling pathway plays a key role in numerous biological and cellular processes, such as cell proliferation, invasion, migration and angiogenesis. It has been found that the lncRNA/PI3K/AKT axis regulates the expression of cancer‑related genes and thus tumour progression. The abnormal regulation of lncRNA expression in the lncRNA/PI3K/AKT axis is clearly associated with clinicopathological features and plays an important role in regulating biological functions. In the present review, the expression and biological functions of PI3K/AKT‑related lncRNAs both <i>in vitro</i> and <i>in vivo</i> over recent years, were comprehensively summarized and analyzed. Their correlation with clinicopathological features was also evaluated, with the objective of furnishing a solid theoretical foundation for clinical diagnosis and the monitoring of efficacy in digestive system neoplasms. The present review aimed to provide a comprehensive overview of the expression and biological functions of PI3K/AKT‑related lncRNAs in digestive system neoplasms and to assess their correlation with clinicopathological features. This endeavor seeks to establish a solid theoretical foundation for the clinical diagnosis and efficacy monitoring of digestive system tumors.</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/PMC11573320/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142604493","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":"An emerging double‑edged sword role of ferroptosis in cardiovascular disease (Review).","authors":"Sirun Qin, Can Zhu, Chenyang Chen, Zhe Sheng, Yu Cao","doi":"10.3892/ijmm.2024.5457","DOIUrl":"10.3892/ijmm.2024.5457","url":null,"abstract":"<p><p>The pathophysiology of cardiovascular disease (CVD) is complex and presents a serious threat to human health. Cardiomyocyte loss serves a pivotal role in both the onset and progression of CVD. Among various forms of programmed cell death, ferroptosis, along with apoptosis, autophagy and pyroptosis, is closely linked to the advancement of CVD. Ferroptosis, a mechanism of cell death, is driven by the buildup of oxidized lipids and excess iron. This pathway is modulated by lipid, amino acid and iron metabolism. Key characteristics of ferroptosis include disrupted iron homeostasis, increased peroxidation of polyunsaturated fatty acids due to reactive oxygen species, decreased glutathione levels and inactivation of glutathione peroxidase 4. Treatments targeting ferroptosis could potentially prevent or alleviate CVD by inhibiting the ferroptosis pathway. Ferroptosis is integral to the pathogenesis of several types of CVD and inhibiting its occurrence in cardiomyocytes could be a promising therapeutic strategy for the future treatment of CVD. The present review provided an in‑depth analysis of advancements in understanding the mechanisms underlying ferroptosis. The present manuscript summarized the interplay between ferroptosis and CVDs, highlighting its dual roles in these conditions. Additionally, potential therapeutic targets within the ferroptosis pathway were discussed, alongside the current limitations and future directions of these novel treatment strategies. The present review may offer novel insights into preventive and therapeutic approaches for CVDs.</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/PMC11573318/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142619693","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] A regulation loop between Nrf1α and MRTF‑A controls migration and invasion in MDA‑MB‑231 breast cancer cells.","authors":"Yao Xu, Ying Luo, Chen Liang, Weibing Xing, Tongcun Zhang","doi":"10.3892/ijmm.2024.5442","DOIUrl":"10.3892/ijmm.2024.5442","url":null,"abstract":"<p><p>Subsequently to the publication of this article, an interested reader drew to the authors' attention that the Control and Nrf1α data panels in Fig. 1G on p. 2463 contained overlapping data, such that these data, which were intended to show the results from differently performed experiments, had apparently been derived from the same original source. Upon examining their original data, the authors realized that the image for the Control experiment was selected incorrectly for this figure. In rectifying this error, the authors have chosen to show the data from one of their repeated experiments for Fig. 1G, and the revised version of this figure is shown on the next page. They can confirm that the replacement of these data in this corrigendum does not significantly affect the conclusions reported in the study. The authors are grateful to the Editor of <i>International Journal of Molecular Medicine</i> for allowing them the opportunity to publish this corrigendum, and wish to apologize to readership for any inconvenience caused. [International Journal of Molecular Medicine 42: 2459‑2468, 2018; DOI: 10.3892/ijmm.2018.3816].</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/PMC11537265/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142499889","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":"Advances in predicting breast cancer driver mutations: Tools for precision oncology (Review).","authors":"Wenhui Hao, Barani Kumar Rajendran, Tingting Cui, Jiayi Sun, Yingchun Zhao, Thirunavukkarasu Palaniyandi, Masilamani Selvam","doi":"10.3892/ijmm.2024.5447","DOIUrl":"10.3892/ijmm.2024.5447","url":null,"abstract":"<p><p>In the modern era of medicine, prognosis and treatment, options for a number of cancer types including breast cancer have been improved by the identification of cancer‑specific biomarkers. The availability of high‑throughput sequencing and analysis platforms, the growth of publicly available cancer databases and molecular and histological profiling facilitate the development of new drugs through a precision medicine approach. However, only a fraction of patients with breast cancer with few actionable mutations typically benefit from the precision medicine approach. In the present review, the current development in breast cancer driver gene identification, actionable breast cancer mutations, as well as the available therapeutic options, challenges and applications of breast precision oncology are systematically described. Breast cancer driver mutation‑based precision oncology helps to screen key drivers involved in disease development and progression, drug sensitivity and the genes responsible for drug resistance. Advances in precision oncology will provide more targeted therapeutic options for patients with breast cancer, improving disease‑free survival and potentially leading to significant successes in breast cancer treatment in the near future. Identification of driver mutations has allowed new targeted therapeutic approaches in combination with standard chemo‑ and immunotherapies in breast cancer. Developing new driver mutation identification strategies will help to define new therapeutic targets and improve the overall and disease‑free survival of patients with breast cancer through efficient medicine.</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/PMC11537269/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142499890","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":"Protective effect of ginseng extract and total ginsenosides on hematopoietic stem cell damage by inhibiting cell apoptosis and regulating the intestinal microflora.","authors":"Zuguo Liang, Xiang Gao, Chenxu Jing, Tongyi Yuan, Lancao Zhang, Yifei Yin, Jianze Ou, Xiangyan Li, Wenxiu Qi, Daqing Zhao, Hang Su, He Zhang","doi":"10.3892/ijmm.2024.5455","DOIUrl":"10.3892/ijmm.2024.5455","url":null,"abstract":"<p><p>Ginseng may improve the myelosuppression and intestinal microbiota disorder induced by cyclophosphamide (CY); however, the effect of ginseng components on hematopoietic stem cell (HSC) damage remains largely unexplored. The present study aimed to assess the protective effect of ginseng extract (GE), total ginsenosides (TG) and total polysaccharides (TP) from ginseng on the intestinal microflora and HSCs of model mice. In the present study, a mouse model of HSC damage induced by CY was constructed, intestinal microflora of fecal samples were sequenced using the 16S ribosomal RNA (rRNA) sequencing techniques, the differentially expressed genes (DEGs) of HSCs were analyzed using high‑throughput RNA‑sequencing, cell apoptosis and erythroid differentiation were detected using flow cytometry and the blood cell parameters were analyzed using a hematology analyzer. Analysis of the 16S rRNA in fecal samples showed that GE, TG and TP improved an imbalanced intestinal microflora, where the relative abundance of <i>Lactobacillus intestinalis</i> had a positive correlation with ginsenosides content. Specifically, TP significantly increased the expression of low‑abundance microflora. Transcriptomic analysis results revealed 2,250, 3,432 and 261 DEGs in the GE, TG and TP groups compared with those in the Model group, respectively. In the expression analysis of DEGs, both TG and GE were found to markedly increase the expression levels of <i>Klf4</i>, <i>Hhex</i>, <i>Pbx1</i>, <i>Kmt2a</i>, <i>Mecom</i>, <i>Zc3h12a</i>, <i>Zbtb16</i>, <i>Lilr4b</i>, <i>Flt3</i> and <i>Klf13</i>. Furthermore, TG inhibited the apoptosis of HSCs by increasing the expression levels of <i>Bcl2</i> and <i>Mcl1</i>, whilst decreasing the expression of <i>Bax</i>. By contrast, GE inhibited the apoptosis of HSCs by reducing the expression of <i>Bax</i> and <i>Bad</i>. Regarding erythroid differentiation and blood cell parameters, GE was found to significantly increase the expression of TER‑119. In addition, GE and TG improved all blood cell parameters, including the count of white blood cells, neutrophils (NEUT), lymphocytes (LYMPH), red blood cells (RBC), hemoglobin (HGB) and reticulocyte and platelets (PLT), whereas TP could only improve the counts of LYMPH, RBC, HGB and PLT. The improvement effect of GE and TG on WBC, NEUT and Ret was superior to TP. In conclusion, TG may protect the hematopoiesis function of HSCs in a CY‑induced mouse model of HSC damage, followed by GE. However, TP did not appear to improve HSC damage. Ginsenosides may therefore be considered essential ingredients in GE when protecting HSCs against damage. GE and TG exerted their protective effects on HSCs by inhibiting the apoptosis of HSCs whilst improving the imbalance of intestinal microflora.</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/PMC11573321/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142604509","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":"Osteosarcoma stem cells resist chemotherapy by maintaining mitochondrial dynamic stability via DRP1.","authors":"Boren Tian, Yaxuan Wu, Xiaoyun Du, Yan Zhang","doi":"10.3892/ijmm.2024.5451","DOIUrl":"10.3892/ijmm.2024.5451","url":null,"abstract":"<p><p>Osteosarcoma malignancy exhibits significant heterogeneity, comprising both osteosarcoma stem cells (OSCs) and non‑OSCs. OSCs demonstrate increased resistance to chemotherapy due to their distinctive cellular and molecular characteristics. Alterations in mitochondrial morphology and homeostasis may enhance chemoresistance by modulating metabolic and regulatory processes. However, the relationship between mitochondrial homeostasis and chemoresistance in OSCs remains to be elucidated. The present study employed high‑resolution microscopy to perform multi‑layered image reconstructions for a quantitative analysis of mitochondrial morphology. The results indicated that OSCs exhibited larger mitochondria in comparison with non‑OSCs. Furthermore, treatment of OSCs with cisplatin (CIS) or doxorubicin (DOX) resulted in preserved mitochondrial morphological stability, which was not observed in non‑OSCs. This finding suggested a potential association between mitochondrial homeostasis and chemoresistance. Further analysis indicated that dynamin‑related protein 1 (DRP1) might play a pivotal role in maintaining the stability of mitochondrial homeostasis in OSCs. Depletion of DRP1 resulted in the disruption of mitochondrial stability when OSCs were treated with CIS or DOX. Additionally, knocking out DRP1 in OSCs led to a reduction in chemoresistance. These findings unveil a novel mechanism underlying chemoresistance in osteosarcoma and suggest that targeting DRP1 could be a promising therapeutic strategy to overcome chemoresistance in OSCs. This provided valuable insights for enhancing treatment outcomes among patients with osteosarcoma.</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/PMC11554380/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142604496","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":"Binding of zebrafish lipovitellin and L1‑ORF2 increases the accessibility of L1‑ORF2 via interference with histone wrapping.","authors":"Ning Ji, Chong-Guang Wu, Wen-Xia Wang, Xiao-Die Wang, Yu Zhai, Luqman Ali, Zhi-Xue Song, Guozhong Zhang, Xu Feng, Yu Wang, Zhan-Jun Lv, Xiufang Wang","doi":"10.3892/ijmm.2024.5443","DOIUrl":"10.3892/ijmm.2024.5443","url":null,"abstract":"<p><p>Long interspersed nuclear element‑1 (L1) is highly expressed in the early embryos of humans, rodents and fish. To investigate the molecular mechanisms underlying high expression of L1 during early embryonic development, a C1‑open reading frame (ORF)2 vector was constructed in which ORF2 of human L1 (L1‑ORF2) was inserted into a pEGFP‑C1 plasmid. C1‑ORF2 vector was injected into early zebrafish embryos (EZEs) to observe expression of EGFP reporter protein by fluorescence microscopy. RNA‑seq and RT‑qPCR were used to detect the effects of lipovitellin (LV)  on gene expression in EZEs. The binding ability of LV to L1‑ORF2 DNA was detected by electrophoretic mobility‑shift assay (EMSA). The chromatin recombinant DNase I digestion and ATAC‑seq assay were used to evaluate the accessibility of plasmid DNA. C1‑ORF2 vector induced high expression of enhanced green fluorescent protein (EGFP) reporter gene after it had been injected into 0 h post‑fertilization (hpf) zebrafish embryos, although histone octamer inhibited expression of EGFP in C1‑ORF2. SDS‑PAGE was used to show that LV was the predominant protein binding ORF2 DNA in 0 hpf zebrafish embryo lysate (ZEL). Both ZEL and purified LV from ZEL attenuated the inhibitory effects induced by histone. LV bound histone to interfere with the binding of histone to ORF2 DNA. Both <i>in vitro</i> chromatin reconstitution experiments and assay for transposase‑accessible chromatin with sequencing with HeLa cells were utilized to demonstrate that the interference induced by LV resulted in increased accessibility of C1‑ORF2. Transcription experiments <i>in vitro</i> verified that LV could enhance the mRNA levels of zebrafish early embryo expression genes grainyhead‑like transcription factor 3 (GRHL3), SRY‑box transcription factor 19a (SOX19A) and nanor (NNR) and also of the EGFP gene. LV was found to increase the expression levels of the zebrafish early embryo expression genes in liver tissue after LV had been injected into the abdominal cavity of adult male zebrafish. Taken together, the findings of the present study demonstrated that LV activates the expression of EGFP induced by ORF2 in EZEs by enhancing the accessibility of ORF2 DNA.</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/PMC11537267/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142499906","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 NEL‑like molecule‑1 in osteogenesis/chondrogenesis (Review).","authors":"Zihan Li, Yihao Tian","doi":"10.3892/ijmm.2024.5446","DOIUrl":"10.3892/ijmm.2024.5446","url":null,"abstract":"<p><p>A dynamic balance exists between osteogenesis and osteoclastogenesis in bone tissue, which can lead to several bone diseases, such as osteoporosis, osteoarthritis, bone necrosis and bone defects, in cases of insufficient osteogenesis or excessive osteoclastogenesis. NEL‑like molecule‑1 (NELL‑1) was first discovered in 1999 as an osteogenic factor that can prevent or treat bone diseases by increasing osteogenic levels. To date, research has identified multiple signaling pathways involved in improving osteogenic levels. Furthermore, to apply NELL‑1 in clinical practice, researchers have optimized its osteogenic effect by combining it with other molecules, changing its molecular structure and performing bone tissue engineering. Currently, research on NELL‑1 is gaining increasing attention. In the near future, it will definitely be applied in clinical practice to eliminate diseases. Thus, the present study provides a comprehensive review of NELL‑1 in enhancing osteogenic levels from the perspectives of the molecular mechanism, interactions with other molecules/cells, molecular‑level changes, applications in bone tissue engineering and its expression in tumors, providing a solid theoretical basis for its clinical application.</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/PMC11537270/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142499908","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}