Signal Transduction and Targeted Therapy最新文献

{"title":"Genome instability goes mobile: damaged DNA transfer between human cells.","authors":"Ashutosh Choudhury, Mathilde Courtes, Nitika Taneja","doi":"10.1038/s41392-026-03030-7","DOIUrl":"10.1038/s41392-026-03030-7","url":null,"abstract":"","PeriodicalId":21766,"journal":{"name":"Signal Transduction and Targeted Therapy","volume":"11 1","pages":""},"PeriodicalIF":81.2,"publicationDate":"2026-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13649729/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149138297","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metabolic immune checkpoints (MICs) in cancer: from molecular mechanisms to challenges and opportunities in clinical translation.","authors":"Jinru Yang, Xing Cai, Fajian He, Junhong Zhang, Ziqiang Zhang, Zongbi Yi, Conghua Xie, Binghe Xu","doi":"10.1038/s41392-026-02903-1","DOIUrl":"10.1038/s41392-026-02903-1","url":null,"abstract":"<p><p>Metabolic reprogramming is a core feature of tumor cells in adapting to microenvironmental stress and acquiring malignant phenotypes. It not only supports rapid proliferation but also mediates immune escape by reshaping the immune microenvironment. In recent years, the \"metabolism-immune axis\", serving as a central hub for the crosstalk between metabolic regulation and immune suppression, has provided a new perspective for understanding tumor immune evasion. This review systematically discusses how metabolic pathways, including glucose, lipid, and amino acid metabolism, along with mitochondrial function and other related processes, shape the immunosuppressive tumor microenvironment by regulating immune cell function, immune checkpoint expression, and immune signaling networks, thereby promoting tumor immune escape. The concept of \"metabolic immune checkpoints (MICs)\" is innovatively proposed and classified into three categories based on their mechanisms of action: (1) MIC-I: metabolic modification-type immune checkpoints, exemplified by posttranslational modifications of immune checkpoint molecules such as PD-L1 lactylation, acetylation and glycosylation, etc.; (2) MIC-II: metabolic enzyme-dependent immune regulatory nodes, represented by enzymes such as indoleamine 2,3-dioxygenase 1 and others that directly influence immune cell function; and (3) MIC-III: microbial metabolite-coupled immune regulatory targets, including receptors for microbe-derived metabolites such as short-chain fatty acid receptors. By integrating molecular interaction networks of key targets such as lactate dehydrogenase A and ATP citrate lyase, this review explores synergistic therapeutic strategies that combine small-molecule inhibitors targeting MICs with immune checkpoint blockade. This highlights how metabolic intervention can restore immune cell function and reverse exhaustion. Current key challenges in clinical translation include limitations in metabolic dynamic monitoring technologies, lack of patient stratification biomarkers and insufficient specificity in microbiome regulation. Future directions will focus on personalized treatment guided by multiomics, integrating single-cell metabolic flux analysis, deep learning-driven target prediction, and synthetic microbiome engineering, driving tumor immunotherapy into the era of precision metabolic regulation. By integrating the fundamental mechanisms of MICs with translational medical research, this review not only provides a systematic paradigm but also establishes a foundation for the development of new-generation precision combination therapies.</p>","PeriodicalId":21766,"journal":{"name":"Signal Transduction and Targeted Therapy","volume":"11 1","pages":""},"PeriodicalIF":81.2,"publicationDate":"2026-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13650150/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149138309","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Circular MIR144 from eccDNA is a superior senescence agonist in aging hearts.","authors":"Ying Zhang, Siyu Wang, Haodong Li, Ying Zhang, Baofeng Yang","doi":"10.1038/s41392-026-02719-z","DOIUrl":"10.1038/s41392-026-02719-z","url":null,"abstract":"","PeriodicalId":21766,"journal":{"name":"Signal Transduction and Targeted Therapy","volume":"11 1","pages":""},"PeriodicalIF":81.2,"publicationDate":"2026-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13658801/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149168958","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SARS-CoV-2 seeds IAPP aggregation and β-cell failure.","authors":"Zhiqi Song, Yanfeng Xu, Wenjie Zhao, Ling Zhang, Yanhong Li, Feifei Qi, Wei Liang, Yunlin Han, Ruolin Wang, Qi Lv, Xujian Liang, Fengdi Li, Ran Deng, Wei Deng, Linlin Bao, Chuan Qin","doi":"10.1038/s41392-026-02914-y","DOIUrl":"10.1038/s41392-026-02914-y","url":null,"abstract":"<p><p>The global diabetes incidence has surged post-COVID-19, yet how SARS-CoV-2 drives long-term beta cell (β-cell) failure remains incompletely elucidated. We identified a mechanism whereby SARS-CoV-2 structural proteins directly hijack islet amyloid polypeptide (IAPP) to induce pathogenic amyloid deposition, disrupting insulin granule maturation, trafficking, and secretion in an age-susceptible islet microenvironment. In macaque models, aged subjects showed extensive islet IAPP aggregation with increased β-cell necroptosis, whereas adult infected animals exhibited minimal IAPP pathology. Multiplex fluorescence in situ hybridization detecting viral sense and antisense RNAs with IAPP immunostaining revealed focal overlap of active viral replication foci with IAPP-rich amyloid regions in aged islets. Molecular docking was used as a hypothesis-generating tool, whereas coimmunoprecipitation, proximity ligation assays, and surface plasmon resonance experimentally confirmed direct spike/nucleocapsid-IAPP binding; interface-guided peptide mutagenesis further showed that five predicted IAPP contact residues are required for binding. Thioflavin-T kinetics and electron microscopy demonstrated that the spike/nucleocapsid markedly accelerated IAPP monomer conversion into dense fibrillar networks. In β cells and primary hIAPP-overexpressing mouse islets, spike/nucleocapsid expression or protein exposure reduced insulin content and induced endoplasmic reticulum stress and inflammatory programs. Integrated spatial islet proteomics linked IAPP-viral complexes to complement activation and vesicle transport dysfunction. Crucially, primary islet qPCR and immunoblotting revealed stalled insulin mRNA with compensatory upregulation of trafficking/exocytosis transcripts but accumulation of insulin precursor proteins, consistent with impaired granule maturation/processing. Thus, SARS-CoV-2 proteins act as pathogenic \"seeds\" for IAPP assembly, establishing an IAPP aggregation-impaired granule maturation-complement activation-vesicle transport blockade axis underlying age-associated vulnerability to post-COVID-19 diabetes.</p>","PeriodicalId":21766,"journal":{"name":"Signal Transduction and Targeted Therapy","volume":"11 1","pages":""},"PeriodicalIF":81.2,"publicationDate":"2026-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13649786/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149138336","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Histone H4K5 lactylation-driven feedback loop modulates glycerol-linked immunosuppressive activity of tumor-associated T regulatory cells.","authors":"Wang Wang, Baida Kong, Changyuan Huang, Ke-Xu Xiong, Chuanxin Su, Yang Lu, Rongzhen Liang, Huimin Wang, Qi Long, Haoran Sun, Qi Hu, Julie Wang, Chuanye Zhang, Wenxi He, Linyu Sha, Yaping Zhi, Chi Zhou, Yiding Xiong, Li Zhou, Xin Chen, Peng Wang, Bing-Hua Jiang, Lianhui Sun, Shimon Sakaguchi, Song Guo Zheng","doi":"10.1038/s41392-026-03039-y","DOIUrl":"10.1038/s41392-026-03039-y","url":null,"abstract":"<p><p>Tumor metastasis is the leading cause of death for more than 90% of cancer patients, with colorectal cancer (CRC) mainly spreading to the liver. The colon and liver possess distinct nutritional microenvironments, yet how these differences shape the tumor immune landscape remains unclear. Using single-cell analysis of autologous samples from CRC patients with liver metastases, we identified a distinct CD177⁺GK⁺ regulatory T (Treg) cell subset in metastatic lesions. Spatial transcriptomics revealed that these GK⁺ Tregs localize at the tumor-adjacent interface and interact with immunosuppressive macrophages. Moreover, a selective clonal selection was observed in the metastatic niche, leading to the super-amplification of metastasis-associated clones of GK⁺ Tregs, suggesting a dominant role of these clones in metastatic immune evasion. Mechanistically, glycerol-derived lactate promotes H4K5 histone lactylation, which upregulates FOXP3 and subsequently GK expression, creating a positive feedback loop that amplifies Treg immunosuppressive activity. Blocking the glycerol metabolic pathway in Tregs combined with anti-PD-1 therapy synergistically curbs tumor progression. Pan-cancer analyses further confirm the potent suppressive activity of CD177⁺GK⁺ Tregs across multiple cancer types. Collectively, our findings highlight glycerol metabolism and histone lactylation as critical drivers of Treg-mediated immune evasion, offering new strategies to reprogram the immunosuppressive tumor microenvironment for enhanced cancer therapy.</p>","PeriodicalId":21766,"journal":{"name":"Signal Transduction and Targeted Therapy","volume":"11 1","pages":""},"PeriodicalIF":81.2,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13645786/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149128626","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Phospholipid phosphatase 2 drives liver repair and regeneration after acute liver injury.","authors":"Fan Li, Yiming Wang, Pengyao Chen, Jiongyuan Li, Hao Wang, Yunyun Xu, Hui Wang, Nan Zhang, Tianning Huang, Yi Wei, Qingfa Bu, Jiahao Si, Jingwen Ma, Xuehao Wang, Qi Ling, Haoming Zhou, Xiaoxiao Liu, Ling Lu, Ming Ni","doi":"10.1038/s41392-026-02825-y","DOIUrl":"10.1038/s41392-026-02825-y","url":null,"abstract":"<p><p>Acute liver injury is commonly caused by overdose-drug, toxins, or ischemia. The liver possesses a remarkable regenerative capacity, wherein metabolic remodeling plays a crucial role in restoring hepatic function and homeostasis. However, the specific metabolic shift that initiates hepatocyte regeneration remains unclear. Here, we employed multi-time-point multi-omics analyses to demonstrate that phosphatidylethanolamine undergoes a dynamic metabolic reprogramming, with phospholipid phosphatase 2 (PLPP2) exhibiting synchronous changes among the enzymes regulating PE metabolism. Liver biopsy samples from patients with drug-induced liver injury corroborated the PLPP2 alterations. In murine models, hepatocyte-specific deletion of PLPP2 exacerbated acute liver injury. Mechanistically, the resolution of ER stress was accompanied by a robust upregulation of PLPP2 during the regenerative phase. This shift promotes liver repair and regeneration by initiating the PE biosynthesis. PE, upon binding to PEBP1, modulated its affinity and strengthened its interaction with GLI1, thereby disrupting the association between lTCH and GLI1 and preventing the ubiquitination and degradation of GLI1. Additionally, PE promotes autophagy by facilitating the lipidation of LC3B. The increase in ER-localized PE mediated by PLPP2 also contributed to the alleviation of ER stress, thus establishing a positive feedback loop. Pharmacologic activation of PLPP2 or supplementation with ethanolamine may represent a promising therapeutic strategy for acute liver injury.</p>","PeriodicalId":21766,"journal":{"name":"Signal Transduction and Targeted Therapy","volume":"11 1","pages":""},"PeriodicalIF":81.2,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13646280/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149127652","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bioengineering strategies for improving the immunogenicity of mRNA vaccines.","authors":"Hong Wang, Ran Zhuo, Junjun Wu, Songying Ouyang","doi":"10.1038/s41392-026-02991-z","DOIUrl":"10.1038/s41392-026-02991-z","url":null,"abstract":"<p><p>Messenger RNA (mRNA) vaccines have reshaped modern vaccinology by enabling rapid antigen design, scalable manufacturing, and coordinated induction of humoral and cellular immunity. Their clinical success has established mRNA as a versatile platform for infectious diseases, cancer immunotherapy, and emerging therapeutic applications. However, expansion into cardiovascular, neurodegenerative, autoimmune, and metabolic disorders imposes indication-specific requirements that cannot be addressed by uniform design strategies. Vaccine performance depends not only on antigen output, but also on how RNA architecture and delivery systems regulate innate sensing, intracellular trafficking, tissue distribution, and adaptive immune programming. In this review, we summarize bioengineering strategies for improving mRNA vaccine immunogenicity by coordinating antigen-expression efficiency with innate immune regulation. We compare non-replicating mRNA, self-amplifying RNA, and circular RNA in terms of expression kinetics, translational logic, safety considerations, and innate immune activation. We then discuss molecular engineering approaches that enhance stability, translation, and immune control, including optimization of cap structures, untranslated regions, poly(A) tails, nucleotide modifications, codon usage, and platform-specific designs for saRNA and circRNA. We further examine delivery systems, including lipid nanoparticles, exosomes, polymer-based carriers, virus-like particles, and hybrid platforms, emphasizing their dual roles in cargo transport and immune modulation. Finally, we discuss indication-specific design principles, manufacturing constraints, and translational challenges. We propose that next-generation mRNA vaccines will require disease-matched co-design of RNA molecules and delivery platforms to enhance antigen expression, tune immune activation, and strengthen clinical translation.</p>","PeriodicalId":21766,"journal":{"name":"Signal Transduction and Targeted Therapy","volume":"11 1","pages":""},"PeriodicalIF":81.2,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13645725/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149128551","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"α7 integrin co-regulates chromatin accessibility and gene expression in HPV-negative head and neck cancer","authors":"Olegs Borodins, Anne Vehlow, Katrin Sameith, Andreas Dahl, Jennifer M. Spangle, Daniela E. Aust, Cornelia Brunner, Outi Monni, Inga Lange, Jovan Mircetic, Elisa Thomas, Nils Cordes","doi":"10.1038/s41392-026-02995-9","DOIUrl":"https://doi.org/10.1038/s41392-026-02995-9","url":null,"abstract":"Epigenetic regulation and gene transcription are dynamically modulated by extracellular signals, including focal adhesions; however, the role of integrins in these processes remains poorly understood. In this study in HPV-negative head and neck squamous cell carcinoma, (HNSCC), we combined investigations in physiological three-dimensional, matrix-embedded cell models and patient-derived organoids with multi-omics analyses, bioinformatics and artificial intelligence, to unmask the integrin effector signaling network that reshapes chromatin to drive cancer. Among the 12 α/β1 integrin receptors, α7 integrin (ITGA7) emerged as the most potent modulator of histone post-translational modifications, associated with significant changes in gene transcription and chromatin accessibility. Depletion of ITGA7, achieved independently by CRISPR/Cas9 knockout and RNA interference, reduced chromatin accessibility at the AURKA locus and downregulated an AURKA-centered transcriptional program. Mechanistically, phosphoproteomics revealed significant inhibition of MAPK- and PI3K/AKT-dependent signaling with concomitant functional impairment of cell cycling and cell survival upon ITGA7 depletion. Across all analyses, machine-learning-based feature selection consistently nominated AURKA as the dominant downstream node, and tumor ITGA7 expression stratified patient overall survival in a non-linear manner. In summary, these findings establish α7 integrin as a key co-regulator of chromatin accessibility and gene transcription in HPV-negative HNSCC, acting through an AURKA-centered axis that couples adhesion signaling to cell cycle control and patient survival, and nominate AURKA, potentially targetable with clinical Aurora-A inhibitors such as alisertib, as an actionable therapeutic node downstream of the currently non-druggable ITGA7.","PeriodicalId":21766,"journal":{"name":"Signal Transduction and Targeted Therapy","volume":"58 1","pages":""},"PeriodicalIF":39.3,"publicationDate":"2026-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149087664","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuro-immune interactions in tumors, immune-related disorders, and infections","authors":"Qing-Yuan Zhuang,Si-Wei Zhang,Zhi-Ming Shao,Yi Xiao,Yi-Zhou Jiang","doi":"10.1038/s41392-026-02842-x","DOIUrl":"https://doi.org/10.1038/s41392-026-02842-x","url":null,"abstract":"Abstract The nervous and immune systems interact to form a complex network that sustains homeostasis and finely tunes immune responses. These interactions significantly influence the pathogenesis and progression of various diseases, such as tumors, immune-related disorders, and infections. Consequently, these interactions have become promising therapeutic targets. However, insufficient mechanistic research and the lack of candidate drugs have restricted the application of therapeutic strategies targeting neuro-immune interactions. In this review, we summarize three modes of neuro-immune interactions: local mechanisms, reflex-level organization, and central nervous system-wide regulation. Next, we elucidate the mechanisms of neuro-immune interactions across different diseases, discuss their variations, and highlight the spatiotemporal heterogeneity of these interactions. Additionally, understanding the dynamic crosstalk between specific neuronal and immune cell subtypes could reveal novel biomarkers and intervention points, facilitating more precise and personalized therapeutic strategies in diverse disease contexts. Furthermore, we dissect the current status of clinical trials and analyze the major challenges hindering effective clinical translation. Finally, we explore the potential of high-throughput sequencing technologies, such as single-cell omics and spatial omics, as well as neuro-electrophysiological methods, for in-depth investigation of related mechanisms. By integrating preclinical and clinical perspectives, this review aims to provide valuable insights into the therapeutic potential and future directions in the burgeoning field of neuro-immune interactions.","PeriodicalId":21766,"journal":{"name":"Signal Transduction and Targeted Therapy","volume":"1 1","pages":""},"PeriodicalIF":39.3,"publicationDate":"2026-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149088750","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Source-specific priming of lung NK cells by Pseudomonas LPS enhances resistance to bacterial pneumonia","authors":"Xin Yang, Haoqi Liu, Quanhui Xu, Jian Peng, Huanxing Sun, Deanna Hausman, Ximing Ran, Erica Herzog, Ye Zhang, F. Susan Wong, Xin Chen, Liqiang Guo, Han Ge, Yanlong Hong, Lei Zhang, Li Wen, Ruirui Wang, Guang Ji","doi":"10.1038/s41392-026-02832-z","DOIUrl":"https://doi.org/10.1038/s41392-026-02832-z","url":null,"abstract":"Bacterial pneumonia is a major cause of morbidity and mortality in elderly individuals, yet how mucosal innate immunity changes with age remains unclear. We detected bacterial DNA, particularly signatures of Pseudomonas, in the circulation of healthy elderly individuals, suggesting that chronic exposure to low-dose microbial components occurs during aging. Using murine models, we found that intratracheal delivery of a low dose of Pseudomonas aeruginosa lipopolysaccharide (LPS) strongly protected against bacterial pneumonia through a microbiota–dependent mechanism, whereas Escherichia coli LPS had no detectable protective effect. This protective response occurred in the absence of adaptive immunity and was mediated by lung–resident natural killer (NK) cells. Transcriptomic profiling revealed that P. aeruginosa LPS selectively upregulated the complement receptor C3aR1 in pulmonary NK cells, increasing their IFN-γ production and LFA-1–dependent adhesion to target cells. Adoptive transfer of P. aeruginosa LPS–conditioned pulmonary NK cells conferred protection to naïve recipients, whereas silencing C3aR1 abrogated this effect. This localized innate training occurred without systemic inflammation and required the presence of a commensal microbiota. These findings reveal that structurally distinct LPS from P. aeruginosa programs lung NK cells toward a C3aR1–driven, high-affinity effector state that enhances resistance to bacterial pneumonia. Source–specific innate conditioning of mucosal NK cells may provide a tissue–targeted strategy to strengthen pulmonary host defense, particularly in aging populations vulnerable to respiratory infections.","PeriodicalId":21766,"journal":{"name":"Signal Transduction and Targeted Therapy","volume":"11 1","pages":""},"PeriodicalIF":39.3,"publicationDate":"2026-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149087697","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}