Molecular Medicine最新文献

{"title":"Tetrandrine induces muscle atrophy involving ROS-mediated inhibition of Akt and FoxO3.","authors":"Xin-Qi Shan, Na Zhou, Chuang-Xin Pei, Xue Lu, Cai-Ping Chen, Hua-Qun Chen","doi":"10.1186/s10020-024-00981-x","DOIUrl":"10.1186/s10020-024-00981-x","url":null,"abstract":"<p><p>Tetrandrine (Tet), a well-known drug of calcium channel blocker, has been broadly applied for anti-inflammatory and anti-fibrogenetic therapy. However, due to the functional diversity of ubiquitous calcium channels, potential side-effects may be expected. Our previous report revealed an inhibitory effect of Tet on myogenesis of skeletal muscle. Here, we found that Tet induced protein degradation resulting in the myofibril atrophy. Upon administration with a relative high dose (40 mg/kg) of Tet for 28 days, the mice displayed significantly reduced muscle mass, strength force, and myosin heavy chain (MyHC) protein levels. The MyHC reduction was further detected in C2C12 myotubes after treating with Tet. Interestingly, the expression of Atrogin-1 and Murf-1, the skeletal muscle specific E3 ligases of protein ubiquitin-proteasome system (UPS), was accordingly up-regulated, and the reduced MyHC was significantly mitigated by MG132, a 26S proteasome inhibitor, indicating a key role of UPS in the protein degradation of muscle cells. Further study showed that Tet induced autophagy also participated in the protein degradation. Mechanistically, Tet treatment caused ROS production in myotubes that in turn targeted on FoxO3/AKT signaling, resulting in the activation of UPS and autophagy processes that were involved in the protein degradation. Our study reveals a potential side-effect of Tet on skeletal muscle atrophy, particularly when the drug dose is relatively high.</p>","PeriodicalId":18813,"journal":{"name":"Molecular Medicine","volume":"30 1","pages":"218"},"PeriodicalIF":6.0,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11566300/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142639346","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Machine learning-driven discovery of novel therapeutic targets in diabetic foot ulcers.","authors":"Xin Yu, Zhuo Wu, Nan Zhang","doi":"10.1186/s10020-024-00955-z","DOIUrl":"10.1186/s10020-024-00955-z","url":null,"abstract":"<p><strong>Background: </strong>To utilize machine learning for identifying treatment response genes in diabetic foot ulcers (DFU).</p><p><strong>Methods: </strong>Transcriptome data from patients with DFU were collected and subjected to comprehensive analysis. Initially, differential expression analysis was conducted to identify genes with significant changes in expression levels between DFU patients and healthy controls. Following this, enrichment analyses were performed to uncover biological pathways and processes associated with these differentially expressed genes. Machine learning algorithms, including feature selection and classification techniques, were then applied to the data to pinpoint key genes that play crucial roles in the pathogenesis of DFU. An independent transcriptome dataset was used to validate the key genes identified in our study. Further analysis of single-cell datasets was conducted to investigate changes in key genes at the single-cell level.</p><p><strong>Results: </strong>Through this integrated approach, SCUBE1 and RNF103-CHMP3 were identified as key genes significantly associated with DFU. SCUBE1 was found to be involved in immune regulation, playing a role in the body's response to inflammation and infection, which are common in DFU. RNF103-CHMP3 was linked to extracellular interactions, suggesting its involvement in cellular communication and tissue repair mechanisms essential for wound healing. The reliability of our analysis results was confirmed in the independent transcriptome dataset. Additionally, the expression of SCUBE1 and RNF103-CHMP3 was examined in single-cell transcriptome data, showing that these genes were significantly downregulated in the cured DFU patient group, particularly in NK cells and macrophages.</p><p><strong>Conclusion: </strong>The identification of SCUBE1 and RNF103-CHMP3 as potential biomarkers for DFU marks a significant step forward in understanding the molecular basis of the disease. These genes offer new directions for both diagnosis and treatment, with the potential for developing targeted therapies that could enhance patient outcomes. This study underscores the value of integrating computational methods with biological data to uncover novel insights into complex diseases like DFU. Future research should focus on validating these findings in larger cohorts and exploring the therapeutic potential of targeting SCUBE1 and RNF103-CHMP3 in clinical settings.</p>","PeriodicalId":18813,"journal":{"name":"Molecular Medicine","volume":"30 1","pages":"215"},"PeriodicalIF":6.0,"publicationDate":"2024-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11562697/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142624150","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Probiotic bacteria-released extracellular vesicles enhance macrophage phagocytosis in polymicrobial sepsis by activating the FPR1/2 pathway.","authors":"Ruiyao Zhu, Yu Zhang, Xiaohong Wang, Benjamin D Liu, Debabrata Chowdhury, Zhixin Li, Mingliang Pan, Tianqing Peng, Jing Chen, Wei Huang, Liying Zhan, Guo-Chang Fan","doi":"10.1186/s10020-024-00959-9","DOIUrl":"10.1186/s10020-024-00959-9","url":null,"abstract":"<p><strong>Background: </strong>Sepsis-induced organ failure and high mortality are largely ascribed to the failure of bacterial clearance from the infected tissues. Recently, probiotic bacteria-released extracellular vesicles (BEVs) have been implicated as critical mediators of intercellular communication which are widely involved in the regulation of the inflammatory response. However, their functional role in macrophage phagocytosis during sepsis has never been explored.</p><p><strong>Methods: </strong>BEVs were collected from three different strains of probiotics including Lactiplantibacillus plantarum WCFS1 (LP WCFS1), Lactobacillus rhamnosus Gorbach-Goldin (LGG), and Escherichia coli Nissle 1917 (EcN), or from LGG cultured under three pH conditions (pH5-acid, pH6.5-standard, pH8-akaline) through differential centrifugation, filtration, and ultracentrifugation of their culture supernatants. In vitro phagocytosis was measured in Raw264.7 cells and bone marrow-derived macrophages using pHrodo red E. coli BioParticles. The in vivo therapeutic effects of BEVs were tested using a feces-injection-in-peritoneum (FIP) model of polymicrobial sepsis.</p><p><strong>Results: </strong>LGG-derived EVs (BEV^LGG) were the best among these three probiotics BEVs in stimulating macrophages to take up bacteria. Furthermore, BEV^LGG collected from pH8 culture condition (BEV^pH8) exhibited the strongest capacity of phagocytosis, compared with BEV^pH5 and BEV^pH6.5. Treatment of septic mice with BEV^pH8 significantly prolonged animal survival; increased bacterial clearance from the blood, peritoneal lavage fluid, and multiple organs; and decreased serum levels of pro-inflammatory cytokines/chemokines, as well as reduced multiple organ injuries, in comparison with control-treated septic mice. Mechanistically, RNA-seq and bioinformatic analysis identified that the FPR1/2 signaling was remarkably activated, along with its downstream pathways (PI3K-Akt-MARCO and NADPH-ROS) in BEV^pH8-treated macrophages, compared with control cells. Accordingly, pre-addition of Boc2, a specific antagonist of FPR1/FPR2, to macrophages significantly attenuated BEV^pH8-mediated phagocytosis, compared to controls.</p><p><strong>Conclusions: </strong>This study demonstrates that LGG-derived BEVs may have therapeutic effects against sepsis-induced organ injury and mortality through enhancing FPR1/2-mediated macrophage phagocytosis.</p>","PeriodicalId":18813,"journal":{"name":"Molecular Medicine","volume":"30 1","pages":"216"},"PeriodicalIF":6.0,"publicationDate":"2024-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11566284/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142624165","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hormonal interventions in skin wounds - a mini review.","authors":"Zeming Li, Rui Ma, Jiajun Tan, Chunmeng Li, Yang Xiao, Xudong Qiu, Shuo Jin, Peng Ouyang, Yiping Zhao, Xiao Xiang, Wang Wu","doi":"10.1186/s10020-024-00978-6","DOIUrl":"10.1186/s10020-024-00978-6","url":null,"abstract":"<p><p>The ability to heal from wounds is perhaps the most important biological function that ensures our survival and perpetuation. Cutaneous wound healing typically consists of four characteristic stages, namely hemostasis, inflammation, proliferation, and remodeling, which are carefully carried out by coordinated actions of various cells, cytokines, and hormones. Incoordination of these steps may impede complete and efficient reconstruction and functional recovery of wounds or even lead to worsened outcomes. Hormones, as powerful modulators of organ functions, participate in multiple steps of the wound healing process and play a pivotal role by choreographing the complex interplay of cellular and molecular events. Leveraging the regulatory effects of hormones to enhance the healing process, hormonal therapy has emerged as a promising approach in the clinical treatment of wounds. Current research has focused on determination of the optimal dosages, delivery methods, and combinations of hormonal therapies to maximize their therapeutic benefits while minimizing potential side effects. This review highlights the molecular mechanisms, clinical benefits and side effects of the most commonly used hormones in clinical treatment of wounds.</p>","PeriodicalId":18813,"journal":{"name":"Molecular Medicine","volume":"30 1","pages":"217"},"PeriodicalIF":6.0,"publicationDate":"2024-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11566089/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142624145","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lipid metabolism-related gene signature predicts prognosis and unveils novel anti-tumor drugs in specific type of diffuse large B cell lymphoma.","authors":"Cancan Wang, Ran Zhang, Huan Zhang, Haixia Gao, Yubing Zhu, Lichao Jiao, Zhiqiang Yi, Meiyu Zhou, Xinxia Li","doi":"10.1186/s10020-024-00988-4","DOIUrl":"10.1186/s10020-024-00988-4","url":null,"abstract":"<p><strong>Background: </strong>Diffuse large B-cell lymphoma (DLBCL) is the most common type of lymphoma which possess highly aggressive and heterogeneous. Despite advances in understanding heterogeneity and development of novel targeted agents, the prognosis of DLBCL patients remains unsatisfied. Lipids are crucial components of biological membranes and signal transduction while accumulating evidence has supported the vital roles of abnormal lipid metabolism in tumorigenesis. Furthermore, some related pathways could serve as prognostic biomarkers and potential therapeutic targets. However, the clinical significance of abnormal lipid metabolism reprogramming in DLBCL has not been investigated. In the current study, we developed a prognostic risk model for DLBCL based on the abnormal expressed lipid metabolism genes and moreover based on our risk model we classified patients with DLBCL into novel subtypes and identified potential drugs for DLBCL patients with certain lipid metabolism profiles.</p><p><strong>Methods: </strong>We utilized univariate Cox regression analysis to identify the prognosis-related lipid metabolism genes, and then performed LASSO Cox regression to identify prognostic related lipid metabolism related genes. Multivariate cox regression was used to establish the prognostic model. Patients were divided in to high and low risk groups based on the median risk score. Immune cell infiltration and GSEA were used to identify the pathways between high and low risk groups. Oncopredict algorithm was utilized to identify potential drug for high-risk patients. In vitro cell apoptosis and viability analysis were employed to verify the specific tumor inhibition effects of AZD5153.</p><p><strong>Results: </strong>Nineteen survival related lipid metabolism genes TMEM176B, LAYN, RAB6B, MMP9, ATAD3B, SLC2A11, CD3E, SLIT2, SLC2A13, SLC43A3, CD6, SIRPG, NEK6, LCP2, CTTN, CXCL2, SNX22, BCL6 and FABP4 were identified and subjected to build the prognostic model which was further verified in four external microarray cohorts and one RNA seq cohorts. Tumor immune microenvironment analysis and GSEA results showed that the activation of MYC targets genes rather than immunosuppression contribute to the poor survival outcome of patients in the high-risk group. AZD5153, a novel bivalent BET bromodomain inhibitor which could inhibit the transcription of MYC and E2F exhibited specific antitumor function for cells with high-risk score.</p><p><strong>Conclusions: </strong>Our results provide the first lipid metabolism-based gene signature for predicting the survival of patients with DLBCL. Furthermore, by determining novel subtypes with our lipid metabolism prognostic model we illustrated that drugs that compromising MYC target genes rather than immune checkpoint inhibitors may be beneficial to DLBCL patients with certain lipid metabolism profiles.</p>","PeriodicalId":18813,"journal":{"name":"Molecular Medicine","volume":"30 1","pages":"210"},"PeriodicalIF":6.0,"publicationDate":"2024-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11559131/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142624148","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: Occurrence and role of Tph cells in various renal diseases.","authors":"Junyi Ren, Kuai Ma, Xiangheng Lu, Haoyu Peng, Jia Wang, Moussa Ide Nasser, Chi Liu","doi":"10.1186/s10020-024-00974-w","DOIUrl":"10.1186/s10020-024-00974-w","url":null,"abstract":"","PeriodicalId":18813,"journal":{"name":"Molecular Medicine","volume":"30 1","pages":"212"},"PeriodicalIF":6.0,"publicationDate":"2024-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11562696/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142624127","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"FTO suppresses cardiac fibrosis after myocardial infarction via m⁶A-mediated epigenetic modification of EPRS.","authors":"Jian Wang, Yanyan Li, Lijie Deng, Yafang Zha, Song Zhang","doi":"10.1186/s10020-024-00985-7","DOIUrl":"10.1186/s10020-024-00985-7","url":null,"abstract":"<p><strong>Background: </strong>Cardiac fibrosis is common in myocardial infarction (MI), leading to progressive cardiac dysfunction. Studies suggested that the abnormal N⁶-methyladenosine (m⁶A) modification induced by fat mass and obesity protein (FTO) is vital in MI. However, the effects of FTO on post-infarction cardiac fibrosis have not been detected.</p><p><strong>Methods: </strong>Western blot and quantitative real-time PCR were performed to detect the expression of FTO in the fibrotic tissue of rats. The functions of FTO on collagen biosynthesis were analyzed in vitro and in vivo. The underlying targets of FTO were selected through RNA-seq with m⁶A-seq. The following dual luciferase reporter assay and RNA stability assay were conducted to investigate the mechanisms of FTO-mediated m⁶A regulation.</p><p><strong>Results: </strong>The expression of FTO was decreased in the fibrotic tissue of post-infarction rats. The HIF-1 signal pathway was enriched after MI. HIF-1α could bind to the promoter of FTO and inhibit its expression. Functionally, FTO inhibited collagen synthesis after MI in vitro and in vivo. Mechanistically, EPRS was selected as the underlying target of FTO-induced m⁶A regulation. IGF2BP3 recognized and bound to the m⁶A sites of EPRS mRNA, which improved its stability. EPRS was required for cardiac fibrosis induced by FTO silencing.</p><p><strong>Conclusions: </strong>FTO, identified as a cardioprotective factor, suppressed collagen synthesis in post-infarction cardiac fibrosis via m⁶A modification, which provided a new therapeutic strategy for cardiac fibrosis.</p>","PeriodicalId":18813,"journal":{"name":"Molecular Medicine","volume":"30 1","pages":"213"},"PeriodicalIF":6.0,"publicationDate":"2024-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11562098/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142624076","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Myc 9aaTAD activation domain binds to mediator of transcription with superior high affinity.","authors":"Andrea Knight, Josef Houser, Tomas Otasevic, Vilem Juran, Vaclav Vybihal, Martin Smrcka, Martin Piskacek","doi":"10.1186/s10020-024-00896-7","DOIUrl":"10.1186/s10020-024-00896-7","url":null,"abstract":"<p><p>The overexpression of MYC genes is frequently found in many human cancers, including adult and pediatric malignant brain tumors. Targeting MYC genes continues to be challenging due to their undruggable nature. Using our prediction algorithm, the nine-amino-acid activation domain (9aaTAD) has been identified in all four Yamanaka factors, including c-Myc. The predicted activation function was experimentally demonstrated for all these short peptides in transactivation assay. We generated a set of c-Myc constructs (1-108, 69-108 and 98-108) in the N-terminal regions and tested their ability to initiate transcription in one hybrid assay. The presence and absence of 9aaTAD (region 100-108) in the constructs strongly correlated with their activation functions (5-, 3- and 67-times respectively). Surprisingly, we observed co-activation function of the myc region 69-103, called here acetyl-TAD, previously described by Faiola et al. (Mol Cell Biol 25:10220-10234, 2005) and characterized in this study as a new domain collaborating with the 9aaTAD. We discovered strong interactions on a nanomolar scale between the Myc-9aaTAD activation domains and the KIX domain of CBP coactivator. We showed conservation of the 9aaTADs in the MYC family. In summary for the c-Myc oncogene, the acetyl-TAD and the 9aaTAD domains jointly mediated activation function. The c-Myc protein is largely intrinsically disordered and therefore difficult to target with small-molecule inhibitors. For the c-Myc driven tumors, the strong c-Myc interaction with the KIX domain represents a promising druggable target.</p>","PeriodicalId":18813,"journal":{"name":"Molecular Medicine","volume":"30 1","pages":"211"},"PeriodicalIF":6.0,"publicationDate":"2024-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11558822/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142624157","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cytokine modulation in pelvic organ prolapse and urinary incontinence: from molecular insights to therapeutic targets.","authors":"Yongxiu Chen, Amin Ullah, Weifang Chen, Jianyan Xuan, Xiaowen Huang, Shiqi Liang, Bairong Shen, Tingfeng Wu","doi":"10.1186/s10020-024-00989-3","DOIUrl":"10.1186/s10020-024-00989-3","url":null,"abstract":"<p><p>Pelvic organ prolapse (POP) and urinary incontinence (UI) are common disorders that significantly impact women's quality of life. Studies have demonstrated that cytokines, including pro- and anti-inflammatory immune mediators, play a role in illness genesis and progression. Research on the inflammatory milieu of the pelvic floor has shown that POP patients have increased inflammation in vaginal tissues. This evidence revealed that significant changes in the inflammatory milieu of the pelvic floor are an aspect of the pathogenesis of POP. POP patients exhibit increased levels of inflammatory cytokines (IL-1, TNF, IFN, and others) in the front vaginal wall, which may alter collagen metabolism and contribute to POP. Studies indicate that cytokines such as IL-6, IL-10, and TGF, which are involved in inflammation, remodelling, and repair, have dual effects on POP and UI. They can promote tissue healing and regeneration but also exacerbate inflammation and fibrosis, contributing to the progression of these conditions. Understanding the dual roles of these cytokines could help us improve the vaginal microenvironment of women and treat POP and UI. Given the considerable changes in these cytokines, this review addresses studies published between 2000 and 2024 on the molecular mechanisms by which pro- and anti-inflammatory cytokines affect women with POP and UI. Furthermore, we explain novel therapeutic strategies for cytokine regulation, emphasizing the possibility of personalized treatments that address the underlying inflammatory milieu of the vagina in POP and UI patients. This thorough analysis aims to establish a foundation for future research and clinical applications, ultimately improving patient outcomes via designed cytokine-based therapies.</p>","PeriodicalId":18813,"journal":{"name":"Molecular Medicine","volume":"30 1","pages":"214"},"PeriodicalIF":6.0,"publicationDate":"2024-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11562709/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142624075","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mesenchymal stem cells lineage and their role in disease development.","authors":"Qi Xu, Wenrun Hou, Baorui Zhao, Peixin Fan, Sheng Wang, Lei Wang, Jinfang Gao","doi":"10.1186/s10020-024-00967-9","DOIUrl":"10.1186/s10020-024-00967-9","url":null,"abstract":"<p><strong>Background: </strong>Mesenchymal stem cells (MSCs) are widely dispersed in vivo and are isolated from several tissues, including bone marrow, heart, body fluids, skin, and perinatal tissues. Bone marrow MSCs have a multidirectional differentiation potential, which can be induced to differentiate the medium in a specific direction or by adding specific regulatory factors. MSCs repair damaged tissues through lineage differentiation, and the ex vivo transplantation of bone marrow MSCs can heal injured sites. MSCs have different propensities for lineage differentiation and pathological evolution for different diseases, which are crucial in disease progression. In this study, we describe various lineage analysis methods to explore lineage ontology in vitro and in vivo, elucidate the impact of MSC lineage differentiation on diseases, advance our understanding of the role of MSC differentiation in physiological and pathological states, and explore new targets and ideas associated with disease diagnosis and treatment.</p>","PeriodicalId":18813,"journal":{"name":"Molecular Medicine","volume":"30 1","pages":"207"},"PeriodicalIF":6.0,"publicationDate":"2024-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11552129/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142624153","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}