Journal of Molecular Medicine-Jmm最新文献

{"title":"Rare and low-frequency variants in families with otitis media.","authors":"Regie Lyn P Santos-Cortez, Christina L Elling, Helen Z Gomez, Elisabet Einarsdottir, Juha Kere, Petri S Mattila, Lena Hafrén, Allen F Ryan","doi":"10.1007/s00109-025-02537-w","DOIUrl":"https://doi.org/10.1007/s00109-025-02537-w","url":null,"abstract":"<p><p>Otitis media is a highly frequent diagnosis in children that causes significant morbidity but remains understudied as a genetic trait despite significant heritability in families. To identify rare or low-frequency variants within genes that confer susceptibility to otitis media, exome sequence data of 287 individuals from 243 families were analyzed. Identified variants were tested for co-segregation with otitis media in family members. Genome sequence data from a case-control cohort was imputed and analyzed for association of specific genes with otitis media. Single-cell RNA-sequence data of identified genes were noted in acutely infected mouse middle ears. Thirty-three variants within 24 genes co-segregated with otitis media in 28 families, of which 18 variants were considered pathogenic or likely pathogenic. An additional 81 variants in 21 of the same genes were identified in 83 unrelated probands with otitis media. Of the 24 genes, 12 were associated with otitis media in mouse models, while 15 genes were replicated from previous human studies. A common variant EYA4 c.829G > A was associated with OM in the case-control cohort. Using network analysis, 22 of the 24 genes were connected in a subnetwork enriched in various signaling pathways, Th1/Th2/Th17 cell differentiation, and viral infections. Majority (87.5%) of the identified genes were expressed in mouse middle ear cells, with differential expression after acute infection. The identification of novel genes and variants for susceptibility to otitis media will be useful in future risk screening and clinical management in children that require a more personalized approach due to poor response to standard treatments. KEY MESSAGES: Thirty-three variants in 24 genes were identified in 28 families with otitis media. Eighteen of these variants within 10 genes were considered (likely) pathogenic. A common variant EYA4 c.829G > A was associated with OM in a case-control cohort. The novel genes were differentially expressed in mouse middle ear post-infection. Genetic screening could identify children for targeted treatment for otitis media.</p>","PeriodicalId":50127,"journal":{"name":"Journal of Molecular Medicine-Jmm","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143781739","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":"Correction to: Traumatic brain injury-induced downregulation of Nrf2 activates inflammatory response and apoptotic cell death.","authors":"Saurav Bhowmick, Veera D'Mello, Danielle Caruso, P M Abdul Muneer","doi":"10.1007/s00109-025-02536-x","DOIUrl":"https://doi.org/10.1007/s00109-025-02536-x","url":null,"abstract":"","PeriodicalId":50127,"journal":{"name":"Journal of Molecular Medicine-Jmm","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143774365","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":"Sphingosine kills Mycobacteria and suppresses mycobacterial lung infections.","authors":"Yuqing Wu, Fabian Schnitker, Yongjie Liu, Simone Keitsch, Federico Caicci, Fabian Schumacher, Andrea Riehle, Barbara Pollmeier, Jan Kehrmann, Burkhard Kleuser, Markus Kamler, Ildiko Szabo, Heike Grassmé, Erich Gulbins","doi":"10.1007/s00109-025-02534-z","DOIUrl":"https://doi.org/10.1007/s00109-025-02534-z","url":null,"abstract":"<p><p>Tuberculous mycobacterial infections pose a substantial global health burden because of their prevalence and multi-drug resistance. The current approach to tackling these infections primarily involves developing new antibiotics or combining existing ones, an approach that often proves ineffective in the specific targeting of mycobacteria. We investigated the effect of sphingosine on tuberculous Mycobacteria in vitro and mycobacterial infections in vivo to test whether sphingosine could potentially be used as a novel drug against tuberculosis. Sphingosine inhibited mycobacterial growth and eradicated mycobacteria in vitro. Mechanistically, sphingosine increased bacterial membrane permeability and induced marked changes on the bacterial plasma membrane evidenced by electron microscopy studies. Administration of sphingosine in a mouse model of pulmonary infection with Bacillus Calmette-Guérin (BCG) greatly reduced the number of bacteria in the lung and prevented pulmonary inflammation. Furthermore, infection of ex vivo human lung tissue samples with BCG and treatment with sphingosine showed that sphingosine also kills BCG in human bronchi. Our findings suggest that sphingosine may be a potential therapeutic intervention against mycobacterial infections. KEY MESSAGES: Sphingosine inhibits mycobacterial growth in vitro. Sphingosine disrupts bacterial membrane integrity. Sphingosine reduces bacterial load in mouse pulmonary infection model. Sphingosine eradicates mycobacteria in human bronchi ex vivo.</p>","PeriodicalId":50127,"journal":{"name":"Journal of Molecular Medicine-Jmm","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143736245","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":"Hepatic microtubule destabilization facilitates liver fibrosis in the mouse model of Wilson disease.","authors":"Som Dev, Yixuan Dong, James P Hamilton","doi":"10.1007/s00109-025-02535-y","DOIUrl":"https://doi.org/10.1007/s00109-025-02535-y","url":null,"abstract":"<p><p>Wilson disease (WD) is a potentially fatal metabolic disorder caused by the inactivation of the copper (Cu) transporter ATP7B, resulting in systemic Cu overload and fibroinflammatory liver disease. The molecular mechanism and effects of elevated Cu on cytoskeletal dynamics in liver fibrogenesis are not clear. Here, we tested the regulation of hepatic cytoskeleton and fibrogenesis with respect to Cu overload in WD. Atp7b^-/- (knockout) mice with established liver disease, hepatocyte-specific Atp7b△^Hep knockout mice without fibroinflammatory disease, and the age-and sex-matched controls were compared using Western blotting, real-time quantitative reverse transcription PCR (qRT-PCR), immunohistochemical (IHC) staining and transcriptomics (RNA-sequencing) analysis. In Atp7b^-/- mice with developed liver disease, there is a significant increase in cytoskeletal protein expression with a reduction in α-tubulin acetylation. In these mice before the onset of liver pathology, no significant changes in cytoskeletal nor hepatic stellate cell activation are observed. As hepatic copper levels rise, an increase in cytoskeletal proteins with a decrease in acetylated-α-tubulin/α-tubulin ratio occurs. RNA-sequencing, qRT-PCR, and immunostaining confirm that the tubulin is upregulated at the transcriptional level and hepatocytes are the primary source of early tubulin increases before fibrosis. An increase in α-tubulin with a decrease in α-tubulin acetylation via Hdac6 and Sirt2 induction facilitates fibrosis as reflected by concomitant increases in desmin and α-SMA immunostaining in Atp7b^-/- mice at 20 weeks. Moreover, strongly positive correlations between α-tubulin and α-tubulin deacetylase with the expression of liver fibrosis markers are observed in animal and human WD. Hepatocyte-specific Atp7b△^Hep mice lack significant changes in tubulin as well as fibrosis despite hepatic steatosis. This study provides evidence that microtubule destabilization causes cytoskeletal rearrangement and facilitates hepatic stellate cell (HSC) activation and fibrosis in the murine model of WD. KEY MESSAGES: Hepatic cytoskeleton system is induced in Wilson disease. Hepatic microtubules acetylation is dysregulated in murine Wilson disease. Microtubules destabilization is positively associated with liver fibrosis in Wilson disease. Microtubules destabilization concomitant with fibrogenesis exacerbates WD progression.</p>","PeriodicalId":50127,"journal":{"name":"Journal of Molecular Medicine-Jmm","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143722359","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":"DNA-RNA hybrids in inflammation: sources, immune response, and therapeutic implications.","authors":"Litao Chen, Lechen Hu, Han Chang, Jianing Mao, Meng Ye, Xiaofeng Jin","doi":"10.1007/s00109-025-02533-0","DOIUrl":"https://doi.org/10.1007/s00109-025-02533-0","url":null,"abstract":"<p><p>Cytoplasmic DNA-RNA hybrids are emerging as important immunogenic nucleic acids, that were previously underappreciated. DNA-RNA hybrids, formed during cellular processes like transcription and replication, or by exogenous pathogens, are recognized by pattern recognition receptors (PRRs), including cGAS, DDX41, and TLR9, which trigger immune responses. Post-translational modifications (PTMs) including ubiquitination, phosphorylation, acetylation, and palmitoylation regulate the activity of PRRs and downstream signaling molecules, fine-tuning the immune response. Targeting enzymes involved in DNA-RNA hybrid metabolism and PTMs regulation offers therapeutic potential for inflammatory diseases. Herein, we discuss the sources, immune response, and therapeutic implications of DNA-RNA hybrids in inflammation, highlighting the significance of DNA-RNA hybrids as potential targets for the treatment of inflammation.</p>","PeriodicalId":50127,"journal":{"name":"Journal of Molecular Medicine-Jmm","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143711967","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":"Mechanism and application of HDAC inhibitors in the treatment of hepatocellular carcinoma.","authors":"Wei Hao, Qingchen Zhang, Yuan Ma, Yue Ding, Chunling Zhao, Chunyan Tian","doi":"10.1007/s00109-025-02532-1","DOIUrl":"https://doi.org/10.1007/s00109-025-02532-1","url":null,"abstract":"<p><p>Hepatoma is the sixth most malignant tumor in the world and the second leading cause of cancer death. Among the types of hepatoma, hepatocellular carcinoma (HCC) is the most important pathological type. For patients with early-stage HCC, the curative treatment is tumor resection. However, early diagnosis and treatment of HCC are difficult; the disease progresses rapidly, and the prognosis is poor. Due to the current limited treatment options for advanced HCC, the identification of new targeted agents is critical for the development of novel approaches to HCC treatment. Histone deacetylases (HDACs) is a protease that removes acetyl groups from histone lysine residues in proteins, and it plays an important role in the structural modification of chromosomes and the regulation of gene expression. Abnormally expressed HDACs can promote tumorigenesis by inducing biological processes such as cell proliferation, migration, and apoptosis inhibition. Since HDACs activity is upregulated in HCC, treatment regimens specifically inhibiting various HDACs have shown good efficacy. This article reviews the application of HDAC inhibitors in the treatment of HCC and explains their mechanisms of action. KEY MESSAGES: HDAC network and cellular effects of HDAC inhibitors. Role and mechanism of HDAC inhibitors in HCC. HDAC inhibitor combined with other ways to treat HCC. The side effects of HDACis in the treatment of HCC.</p>","PeriodicalId":50127,"journal":{"name":"Journal of Molecular Medicine-Jmm","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143711969","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":"Regulation of innate lymphoid cell by microbial metabolites.","authors":"Hongji Tao, Jingjing Geng, Long Bai, Dan Su, Yu Zhao, Guifang Xu, Mingming Zhang","doi":"10.1007/s00109-025-02530-3","DOIUrl":"https://doi.org/10.1007/s00109-025-02530-3","url":null,"abstract":"<p><p>Innate lymphoid cells (ILCs) are a unique category of immune cell that lack antigen-specific receptors yet possess the capacity to detect signals from the surrounding tissue. The majority of ILCs reside in the lymphoid and mucosal tissues, maintaining close associations with the microbiota. Beyond the contributions of accessory cells and adaptive immune cells, accumulating studies demonstrate that microbial metabolites serve a crucial role in mediating the relationship between ILCs and the microbiota. In this review, we highlight and summarize the roles of microbial metabolites from different sources in modulating ILC subsets, proposing these metabolites as potential therapeutic mechanisms in ILC-mediated diseases.</p>","PeriodicalId":50127,"journal":{"name":"Journal of Molecular Medicine-Jmm","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143702069","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":"SMARCC1 promotes M2 macrophage polarization and reduces ferroptosis in lung cancer by activating FLOT1 transcription.","authors":"Youliang Tao, Huafeng Ji, Wensheng Hu, Guojun Jiang, Fangding Yang, Xu Peng, Xu Zhang, Yuqin Yin, Zhize Yuan, Dukai Chen","doi":"10.1007/s00109-025-02531-2","DOIUrl":"https://doi.org/10.1007/s00109-025-02531-2","url":null,"abstract":"&lt;p&gt;&lt;p&gt;Grounded on the bioinformatics insights, this study explores the role of flotillin 1 (FLOT1) in modulating macrophage phenotype and immune evasion in lung cancer cells. The bioinformatics analyses revealed positive correlations between FLOT1 expression and infiltration of M2 macrophages, neutrophils, dendritic cells, and CD4 memory T cells. Furthermore, elevated FLOT1 expression was associated with a poor prognosis in lung cancer patients. Analysis of tumor and adjacent non-tumor tissues from 53 lung cancer patients revealed significantly higher immunohistochemical staining of FLOT1 in tumor tissues, showing positive correlation with the staining intensity of PD-L1. Additionally, staining intensities for markers of M2 macrophages (Arg1), CD4 memory T cells (CD4), dendritic cells (CD83), and neutrophils (CD177) were significantly higher in tumor tissues with high FLOT1 levels. Silencing of FLOT1 was induced in two lung cancer cell lines. Co-culturing in conditioned media of the FLOT1-silenced cancer cells led to reduced chemotactic migration and M2 skewing of macrophages in vitro. Using xenograft models, we observed that FLOT1 silencing weakened tumorigenic activity of A549 cells in mice and reduced M2 macrophage infiltration in tumors. SWI/SNF related BAF chromatin remodeling complex subunit C1 (SMARCC1) was identified as a transcription factor that activated FLOT1 transcription by binding to its promoter. Knockdown of SMARCC1 in lung cancer cells similarly reduced the migration and M2 polarization of macrophages as well as weakened tumorigenesis in mice. However, these effects were counteracted by FLOT1 overexpression. Further analysis of the downstream effectors of the SMARCC1/FLOT1 cascade revealed the enrichment of these factors in ferroptosis-related pathways. Mechanistically, SMARCC1 knockdown led to a decreased GSH:GSSG ratio and increased lipid peroxidation in macrophages, while FLOT1 overexpression restored these changes. Transmission electron microscopic observation revealed typical features of ferroptosis-resistant mitochondria following SMARCC1 knockdown, including fragmented or reduced cristae and increased outer membrane integrity. These mitochondrial changes were mitigated by FLOT1 overexpression. In conclusion, SMARCC1 promotes immune evasion in lung cancer by activating FLOT1 transcription. This activation enhances recruitment and M2 polarization of macrophages, and increases PD-L1 expression, reduces ferroptosis. These findings provide valuable insights into the molecular mechanisms of immune evasion and suggest potential therapeutic targets for lung cancer treatment. KEY MESSAGES: • FLOT1 is associated with poor prognosis in lung cancer patients. • Association between FLOT1 and immune cell infiltration in lung cancer. • Silencing FLOT1 inhibits the recruitment of macrophages by lung cancer cells. • SMARCC1 is highly expressed in lung cancer and promotes the transcription of FLOT1. • FLOT1 overexpression rescues the inhibi","PeriodicalId":50127,"journal":{"name":"Journal of Molecular Medicine-Jmm","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143665235","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":"Targeting ferroptosis for the treatment of female reproductive system disorders.","authors":"Rui Ye, Yi-Ming Mao, Yi-Ran Fei, Yue Shang, Ting Zhang, Zhe-Zhong Zhang, Yong-Lin Liu, Jun-Yu Li, Shi-Liang Chen, Yi-Bo He","doi":"10.1007/s00109-025-02528-x","DOIUrl":"https://doi.org/10.1007/s00109-025-02528-x","url":null,"abstract":"<p><p>Ferroptosis, a regulated form of cell death driven by iron-dependent lipid peroxidation, has emerged as a critical factor in female reproductive health and has been implicated in disorders such as polycystic ovary syndrome, premature ovarian insufficiency, endometriosis, and ovarian cancer. This review explores the intricate molecular mechanisms underlying ferroptosis, emphasizing its reliance on iron metabolism and oxidative stress, which disrupt key processes in reproductive tissues, including granulosa cell function, folliculogenesis, and embryo implantation. Increasing evidence linking ferroptosis to these conditions offers new therapeutic opportunities, with iron chelators, lipid peroxidation inhibitors, and antioxidants showing the potential to alleviate reproductive dysfunction by modulating ferroptotic pathways. In ovarian cancer, ferroptosis inducers combined with conventional cancer therapies, such as chemotherapy, provide promising strategies to overcome drug resistance. This review synthesizes current knowledge on ferroptosis and highlights its importance as a therapeutic target in reproductive health, emphasizing the need for further research to refine and expand treatment options, evaluate their applicability in clinical settings, and explore their role in fertility preservation. By advancing our understanding of ferroptosis regulation, these therapeutic approaches could lead to novel treatments for reproductive disorders and cancers, offering new hope for improving outcomes in women's health and cancer therapy.</p>","PeriodicalId":50127,"journal":{"name":"Journal of Molecular Medicine-Jmm","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143659284","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":"Regulatory role of annexin A1 in NLRP3 inflammasome activation in atopic dermatitis: insights from keratinocytes in human and murine studies.","authors":"Rebeca D Correia-Silva, Mab P Corrêa, Maria Eduarda de Castro, Joaquim S Almeida, Solange C G P D'Ávila, Sonia M Oliani, Karin V Greco, Cristiane D Gil","doi":"10.1007/s00109-025-02529-w","DOIUrl":"https://doi.org/10.1007/s00109-025-02529-w","url":null,"abstract":"<p><p>Despite the well-documented regulatory role of annexin A1 (ANXA1) in numerous stages of the inflammatory response, its involvement in regulating the NLRP3 inflammasome in the context of allergic responses has not been extensively investigated to date. This study evaluated the expression patterns of the ANXA1 and NLRP3 proteins in human skin samples obtained from patients with atopic dermatitis (AD) and in mice with ovalbumin (OVA)-induced experimental AD. Furthermore, the in vitro effect of the ANXA1 mimetic peptide Ac2-26 on IL-4-stimulated human keratinocytes was evaluated. IL-4-stimulated keratinocytes were treated with Ac2-26 (a mimetic peptide of ANXA1) in two different concentrations: 5 and 25 ng/mL. Additionally, some cells were treated with the pan-formyl peptide receptor antagonist Boc2 at a concentration of 10 µM, administered 15 min before Ac2-26. The NLRP3 protein demonstrated intense immunoreactivity in both murine and human AD skin samples, with NLRP3 and ANXA1 exhibiting particularly high coexpression in keratinocytes. A significant increase in ANXA1 and NLRP3 transcripts was observed in AD skins (GSE16161 study). ANXA1 transcript levels were elevated in the AD epidermis relative to the non-lesional epidermis, while NLRP3 transcript levels were reduced in the AD epidermis (GSE120721 study). The Ac2-26 treatment reduced the proliferation rate of IL-4-stimulated keratinocytes, an effect abolished by Boc2 and IL-1β and ROS production. In conclusion, our findings indicate that ANXA1 plays a role in regulating NLRP3 activation in keratinocytes, contributing to the pathogenesis of AD. KEY MESSAGES: ANXA1 and NLRP3 levels are upregulated and exhibit coexpression in murine and human AD skins. ANXA1-FPR axis regulates the proliferation of human keratinocytes under IL-4 stimulation. ANXA1-derived peptide Ac_2-26 regulates oxidative stress and NLRP3 activation in human keratinocytes.</p>","PeriodicalId":50127,"journal":{"name":"Journal of Molecular Medicine-Jmm","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143659055","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}