Interdisciplinary Medicine最新文献

{"title":"Biomimetic mineralization-inspired formulation-adjuvant integrated circRNA nanovaccine against COVID-19","authors":"Liangru Lin,&nbsp;Yingying Ren,&nbsp;Jing Li,&nbsp;Panxing Ren,&nbsp;Xinran Wang,&nbsp;Yixin Ding,&nbsp;Linsu Liu,&nbsp;Cong Liu,&nbsp;Zhou Li,&nbsp;Yan Liu,&nbsp;Dan Luo","doi":"10.1002/inmd.70135","DOIUrl":"https://doi.org/10.1002/inmd.70135","url":null,"abstract":"<p>Conventional RNA-based vaccines rely on lipid nanoparticles (LNPs) for delivery; however, concerns exist regarding the potential systemic toxicity of their chemical composition, and their immune-activating capabilities require further enhancement. Inspired by Mg²⁺ as a key ion for maintaining RNA secondary structure stability, we developed a one-pot method for directly synthesizing a circular RNA-based formulation-adjuvant integrated nanovaccine (CircRNA@FAiNVac) capable of delivering programmed circular RNA (circRNA) based on biomimetic mineralization principles. Specifically, during circRNA rolling circle transcription, the controllable crystallization of magnesium pyrophosphate (MgPPi) nanoparticles was achieved by enhancing the reaction kinetics between ribonucleotide triphosphates and Mg²⁺, thereby encapsulating circRNA within the nanoparticles and forming a protective carrier that also functions as an adjuvant. Based on the specific hydrolysis of MgPPi by pyrophosphatase, CircRNA@FAiNVac can efficiently release RNA intracellularly, thereby facilitating gene expression. Unlike LNPs, which often contain toxic excipients, the vector structure of CircRNA@FAiNVac consisted only of nucleic acid precursors and ions, exhibiting good biocompatibility and reducing adverse reactions. More importantly, CircRNA@FAiNVac possessed potent immune activation capabilities; its self-adjuvanting activity promoted multimodal immune activation, enhancing both humoral and cellular responses. Animal experiments confirmed that the innovative design of CircRNA@FAiNVac ensured stable and sustained autonomous expression of the SARS-CoV-2 receptor-binding domain, while the nanostructure activated multiple immune pathways, providing potent protection. The formulation-adjuvant integration strategy of CircRNA@FAiNVac based on biomimetic mineralization principles provides an alternative approach for the development of next-generation vaccines. Based on antigen sequence optimization, it enables rapid customized development of vaccines targeting variant strains.</p>","PeriodicalId":100686,"journal":{"name":"Interdisciplinary Medicine","volume":"4 5","pages":""},"PeriodicalIF":13.6,"publicationDate":"2026-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/inmd.70135","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148994602","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting the intratumoral microbiota to overcome cancer immunotherapy resistance (5/2026)","authors":"Bufu Tang,&nbsp;Tong Jiang,&nbsp;Yaling Lin,&nbsp;Wei Zhang,&nbsp;Hongjie Fan,&nbsp;Minjie Yang,&nbsp;Bingzhe Li,&nbsp;Yaozu Liu,&nbsp;Changyu Li,&nbsp;Xuran Jin,&nbsp;Wen Zhang,&nbsp;Zhiping Yan,&nbsp;Qianqian Zhao,&nbsp;Xuefeng Kan,&nbsp;Xudong Qu","doi":"10.1002/inmd.70174","DOIUrl":"https://doi.org/10.1002/inmd.70174","url":null,"abstract":"<p>This cover depicts an upward-looking abyssal scene. Copper-dark gold pathogenic bacteria twine around glowing immune cells, illustrating that harmful intratumoral bacteria lead to T cell exhaustion and immunotherapy resistance. Clustered pathogens form shadow silhouettes to represent tumor immune escape. The light shining down from the top symbolizes therapeutic strategies: removing harmful bacteria and utilizing beneficial microbes as well as their metabolites to restore anti-tumor immunity. The image straightforwardly demonstrates the bidirectional interactions between intratumoral microbes, tumor cells and immune cells, showcasing interdisciplinary research on cancer immunotherapy.\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":100686,"journal":{"name":"Interdisciplinary Medicine","volume":"4 5","pages":""},"PeriodicalIF":13.6,"publicationDate":"2026-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/inmd.70174","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148994643","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sel1l preserves condylar cartilage matrix homeostasis by regulating PERK signaling","authors":"Xinqi Huang,&nbsp;Zinan Cen,&nbsp;Zhihe Zhao,&nbsp;Xiao Cen","doi":"10.1002/inmd.70130","DOIUrl":"https://doi.org/10.1002/inmd.70130","url":null,"abstract":"<p>Temporomandibular joint osteoarthritis (TMJOA) is a degenerative disease with orofacial pain and impaired joint function. However, the mechanisms are not well understood. Sel1l-mediated endoplasmic reticulum-associated degradation (ERAD) orchestrates protein homeostasis. Here, we investigated the roles and mechanisms of Sel1l-mediated ERAD in TMJOA induced by complete Freund's adjuvant injection and disc displacement. The osteoarthritic cartilage presented dysregulated ERAD signaling, and the expression of Sel1l was decreased in early OA condition. Intra-articular injection of sh-Sel1l adeno-associated virus induced cartilage catabolism. The RNA-sequencing data and immunofluorescence staining also showed the upregulation of genes related to extracellular matrix (ECM) degradation, while the downregulation of genes associated with chondrogenic differentiation in Sel1l-depleted chondrocytes. These results indicate that Sel1l deficiency induced cartilage catabolism both in vivo and in vitro. Mechanistically, Sel1l-depleted chondrocytes were revealed to harbor excessive endoplasmic reticulum (ER) stress, especially mediated by PERK activation. PERK inhibition suppressed the expression of ER stress markers, rescued the ECM degradation of Sel1l-depleted condylar chondrocytes, and relieved the TMJOA pathogenesis.</p>","PeriodicalId":100686,"journal":{"name":"Interdisciplinary Medicine","volume":"4 5","pages":""},"PeriodicalIF":13.6,"publicationDate":"2026-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/inmd.70130","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148993937","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metabolic feature profiling and metabolic vulnerability in acute lymphoblastic leukemia","authors":"Xiaojie Liang,&nbsp;Zihong Cai,&nbsp;Bingqing Tang,&nbsp;Zicong Huang,&nbsp;Baiwei Luo,&nbsp;Bingyu Lin,&nbsp;Yunong Yang,&nbsp;Zhihao Jin,&nbsp;Xiaoqing Li,&nbsp;Xiuli Xu,&nbsp;Yeling Deng,&nbsp;Chaoran Lin,&nbsp;Liang Wang,&nbsp;Hongsheng Zhou","doi":"10.1002/inmd.70134","DOIUrl":"https://doi.org/10.1002/inmd.70134","url":null,"abstract":"<p>Metabolic reprogramming is a hallmark of cancer and serves as a potential therapeutic target, whereas the metabolic feature of acute lymphoblastic leukemia (ALL) was marginally addressed. Based on RNA-sequencing data in an in-house and external cohort, we aimed to dissect metabolic feature subtypes (MFS) of ALL, which were further cross-validated through a transcriptomics-metabolomics-functional systematic framework. ALL were stratified into three subtypes, of which MFS1 was polysaccharide-metabolic, MFS2 was cold-metabolic, and MFS3 was glycolysis hot-metabolic subtype. Notably, metabolic stratification was significantly associated with patient survival, as 70%–81% overall-survival in MFS1, compared with 25%–56% in MFS2 and MFS3 (MFS1 vs. MFS2, MFS3, <i>p</i> &lt; 0.001). Additional analysis revealed the association between MFSs and clinical features, molecular mutation, and copy number aberration. Metabolic heterogeneity indicated susceptibility to antimetabolite drugs for ALL in vitro. MFS1 was sensitive to antimetabolite drugs for ALL, such as L-asparaginase and 6-mercaptopurine, while MFS2 and MFS3 were resistant. Furthermore, a glycolysis inhibitor reversed the resistance to L-asparaginase and promoted survival in MFS3-patient-derived xenografts. We developed a novel metabolic-stratification, which dissects metabolic profiling, clinical outcome, and therapeutic vulnerability for precision metabolic intervention in ALL.</p>","PeriodicalId":100686,"journal":{"name":"Interdisciplinary Medicine","volume":"4 5","pages":""},"PeriodicalIF":13.6,"publicationDate":"2026-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/inmd.70134","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148994309","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrated one-pot CRISPR-Cas detection: Addressing strategies and future prospects","authors":"Jian Zhou,&nbsp;Xuemei Ren,&nbsp;Yingjie Ren,&nbsp;Ruiping Wu,&nbsp;Ruiman Geng,&nbsp;Le Chen,&nbsp;Zhuo Li","doi":"10.1002/inmd.70158","DOIUrl":"https://doi.org/10.1002/inmd.70158","url":null,"abstract":"<p>Integrated one-pot CRISPR-Cas detection combines isothermal amplification with CRISPR-Cas-mediated recognition in a single vessel, streamlining workflows, reducing time, and minimizing contamination risks for point-of-care diagnostics. This review systematically outlines current advances and core challenges, focusing on strategies to enhance performance. Existing methods achieve temporal and spatial coordination of amplification and detection through physical compartmentalization, chemical regulation, or enzymatic modulation, effectively mitigating interference between Cas enzymes and amplification systems to boost sensitivity and reliability. Despite progress, issues remain in system compatibility, multiplexing, sample matrix interference, and portable quantitative readouts. Future progress will rely on protein engineering for optimized Cas variants, artificial intelligence-assisted crRNA design, fully integrated microfluidic devices with lyophilized reagents, and non-optical detection modalities such as electrochemical or colorimetric.</p>","PeriodicalId":100686,"journal":{"name":"Interdisciplinary Medicine","volume":"4 5","pages":""},"PeriodicalIF":13.6,"publicationDate":"2026-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/inmd.70158","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148994319","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Black phosphorus-based photothermal disruption of cancer-associated fibroblast barriers and tumor-associated macrophage targeting to enhance anti-PD-L1 immunotherapy in triple-negative breast cancer","authors":"Bo Pan,&nbsp;Shicui Hong,&nbsp;Xinyue Wang,&nbsp;Yanghang Li,&nbsp;Cai Wang,&nbsp;Yaxiao Liu,&nbsp;Ying Chen,&nbsp;Chen Fang,&nbsp;Yifeng Zheng,&nbsp;Shengqi Wang,&nbsp;Juping Zhang,&nbsp;Neng Wang,&nbsp;Zhiyu Wang","doi":"10.1002/inmd.70136","DOIUrl":"https://doi.org/10.1002/inmd.70136","url":null,"abstract":"<p>Triple-negative breast cancer (TNBC) remains a clinical challenge due to its high risk of recurrence and metastasis, coupled with limited responses to immunotherapy. Tumor-associated macrophages (TAMs) contribute to immunosuppression in the tumor microenvironment (TME) through C-X-C motif ligand 1 (CXCL1) secretion, but their targeting is hindered by poor drug delivery efficiency and physical barriers imposed by cancer-associated fibroblasts (CAFs). To address this, we developed a TAM-targeting black phosphorus nanosystem (αM2-BP-BHS, MBB) loaded with Baohuoside I (BHS), a known inhibitor of TAM polarization and CXCL1 secretion. In vitro and in vivo studies demonstrated that MBB efficiently targets TAMs and penetrates CAF barriers via photothermal activation under 808 nm near-infrared (NIR) irradiation, significantly enhancing BHS-mediated suppression of TAM/CXCL1 signaling. Furthermore, MBB-mediated photothermal therapy (PTT) boosted the memory T cell population, CD8⁺ T-cell infiltration and cytotoxic cytokine expression. When combined with anti-PD-L1 therapy, MBB synergistically suppressed TNBC progression and metastasis while establishing durable anti-cancer immunity to prevent recurrence. Notably, MBB exhibited excellent biocompatibility with minimal off-target effects, underscoring its potential as a precision delivery platform for BHS. Our findings highlight MBB as a promising adjuvant to potentiate immunotherapy in TNBC by concurrently overcoming stromal resistance and reprogramming immunosuppressive TME.</p>","PeriodicalId":100686,"journal":{"name":"Interdisciplinary Medicine","volume":"4 5","pages":""},"PeriodicalIF":13.6,"publicationDate":"2026-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/inmd.70136","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148994601","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Macrophage extracellular vesicles deliver Mef2d proteins to aggravate Bacteroides fragilis pathogenicity in type 2 diabetes arterial calcification","authors":"Cong Chen,&nbsp;Rong He,&nbsp;Jirong Luo,&nbsp;Zhengfeng Liang,&nbsp;Qunwen Pan,&nbsp;Shuangquan Liu,&nbsp;Jingsong Cao","doi":"10.1002/inmd.70121","DOIUrl":"https://doi.org/10.1002/inmd.70121","url":null,"abstract":"<p>Gut dysbiosis is tightly linked to type 2 diabetes (T2D) arterial calcification (AC), but the mechanism of gut dysbiosis remains poorly defined. Here, we found that a T2D AC associated-gut <i>Bacteroides</i> <i>fragilis</i> (BF) was activated by M1 macrophage-derived extracellular vesicles (EVs). BF internalized macrophage EVs via membrane protein OprM-Jup interaction. Upon uptake, Mef2d, which was rich in EVs, translocated to the BF nucleoid and suppressed ArsR family transcriptional regulator (ArsR) transcription and enhanced BF proliferation and trimethylamine N-oxide production in diabetic mice. Mechanistically, Mef2d suppressed the transcriptional activity of ArsR, an arsenic resistance regulator in BF. Overexpression of ArsR inhibited BF growth and trimethylamine synthesis, whereas ArsR knockdown exacerbated these phenotypes. Critically, ArsR overexpression abolished macrophage EV-driven BF activation. Our findings reveal a macrophage EV-BF signaling axis in which Mef2d-mediated ArsR suppression drives bacterial pathogenicity, offering a pharmacologically targetable axis for precision inhibitation of BF pathobiont virulence in diabetic complications.</p>","PeriodicalId":100686,"journal":{"name":"Interdisciplinary Medicine","volume":"4 5","pages":""},"PeriodicalIF":13.6,"publicationDate":"2026-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/inmd.70121","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148999111","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Implantable drug delivery system: Frontiers of medicine-engineering interdisciplinary","authors":"Yu Zeng,&nbsp;Rongtai Su,&nbsp;Manyu Zhao,&nbsp;Xin Song,&nbsp;Ran Liu,&nbsp;Yuhao Zhou,&nbsp;Chaojuan Yang,&nbsp;Yanli Jiao,&nbsp;Xiao-Wei Xiang,&nbsp;Lingqian Chang","doi":"10.1002/inmd.70133","DOIUrl":"https://doi.org/10.1002/inmd.70133","url":null,"abstract":"<p>Conventional drug delivery methods, such as oral administration and intravenous injection, are associated with several challenges including high systemic toxicity, difficulty in dosage control, and delayed therapeutic responses. These issues limit both the efficacy of treatments and patient compliance, thus becoming a bottleneck in the advancement of precision medicine. In recent years, implantable drug delivery systems (IDDS) have emerged as a promising frontier at the intersection of precision medicine and medical engineering. Through in vivo implantation coupled with signal response mechanisms, IDDS facilitates targeted drug delivery, dynamic regulation, and real-time responsiveness. These significantly enhance therapeutic efficacy while reducing toxicity levels, offering a new path to address the limitations inherent in traditional delivery methods. This article reviews the research progress of IDDS. The technical principles and module innovations are systematically elaborated based on three mechanisms: endogenous response, exogenous triggering, and closed-loop control. Furthermore, it explores the pivotal role that flexibilization and miniaturization of IDDS play in improving biocompatibility, tissue adhesion capabilities, and spatial adaptability. The article also summarizes application examples within typical disease models while analyzing core challenges related to clinical translation. Finally, it anticipates future development directions for integrating medical engineering into this evolving field.</p>","PeriodicalId":100686,"journal":{"name":"Interdisciplinary Medicine","volume":"4 4","pages":""},"PeriodicalIF":13.6,"publicationDate":"2026-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/inmd.70133","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148532830","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multimodal MRI and multiomics reveal high-risk neurophenotype in brain-gut circuits as therapeutic target for Crohn's disease","authors":"Xuehua Li,&nbsp;Ruonan Zhang,&nbsp;Xiaodi Shen,&nbsp;Shaochun Lin,&nbsp;Chuhuai Wang,&nbsp;Weikai Zheng,&nbsp;Weimiao Kong,&nbsp;Zihao Lin,&nbsp;Rongchang Li,&nbsp;Caiguang Liu,&nbsp;Xin Cao,&nbsp;Li Huang,&nbsp;Weitao He,&nbsp;Jinjiang Lin,&nbsp;Haijie Wang,&nbsp;Zhoulei Li,&nbsp;Marietta Iacucci,&nbsp;Subrata Ghosh,&nbsp;Zhenpeng Peng,&nbsp;Canhui Sun,&nbsp;Minhu Chen,&nbsp;Guang Yang,&nbsp;Yejun Wang,&nbsp;Ren Mao,&nbsp;Shi-Ting Feng","doi":"10.1002/inmd.70122","DOIUrl":"https://doi.org/10.1002/inmd.70122","url":null,"abstract":"<p>The brain-gut axis shapes Crohn's disease (CD) pathogenesis, yet CD-associated neurophenotypes lack defined clinical and mechanistic significance. This work aimed to define these neurophenotypes, assess their prognostic impact, elucidate neurophenotype-driven progression mechanisms using multi-omics, and validate their therapeutic potential in vivo. 109 CD patients were prospectively recruited from two centers and underwent baseline multimodal neuro-MRI, MR enterography, ileocolonoscopy, and fecal/blood sample collection. The neurophenotypes were characterized using a multimodal neuro-MRI model developed from 13 of 13,870 features. 83 patients were followed up for disease progression, with repeated brain-gut assessments. Multi-omics (fecal microbiome/metabolomics, serum metabolomics/neurotransmitters) were used to decode the mechanisms underlying neurophenotype-driven progression. Dextran sulfate sodium (DSS)-induced colitis mice with different neurophenotypes were treated with repeated transcranial magnetic stimulation (rTMS) to explore its therapeutic potential. Multimodal neuro-MRI accurately mapped CD-specific neural signatures, stratifying patients into high-risk (neurophenotype score ≥ 0.45) and low-risk neurophenotypes with robust cross-center validity (training cohort AUC = 0.842, test cohort AUC = 0.824). High-risk neurophenotype was identified as an independent predictor of accelerated disease progression (Hazard ratio = 15.46, <i>p</i> = 0.030), independent of intestinal inflammation. Integrated multi-omics revealed that the high-risk neurophenotype contributed to CD progression through microbial-metabolic-neurotransmitter networks where tryptophan emerged as the central regulatory hub. Serum tryptophan levels were negatively correlated with neurophenotype severity and intestinal disease progression. rTMS targeting high-risk neurophenotype in DSS-induced colitis mice elevated tryptophan levels and ameliorated intestinal disease activity. This study redefines the high-risk neurophenotype as a sustained pathogenic driver rather than a mere phenomenon, proposing brain-gut axis modulation as a promising therapeutic strategy distinct from conventional anti-inflammatory approaches.</p>","PeriodicalId":100686,"journal":{"name":"Interdisciplinary Medicine","volume":"4 4","pages":""},"PeriodicalIF":13.6,"publicationDate":"2026-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/inmd.70122","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148532867","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Artificial cell: An emerging bioactive material with advanced applications in cancer theranostics","authors":"Daikun Wu,&nbsp;Shuo Yang,&nbsp;Hongjing Dou","doi":"10.1002/inmd.70139","DOIUrl":"https://doi.org/10.1002/inmd.70139","url":null,"abstract":"<p>Artificial cells have emerged as a class of promising bioactive materials that recapitulate key structural and functional features of natural cells, serving as an effective alternative to address the inherent bottlenecks of conventional biomaterials in biomedical research, particularly in cancer theranostics. Fabricated primarily via bottom-up strategies, these bioactive constructs enable modular assembly of functional biomaterials to build hierarchical systems spanning artificial organelles, diverse artificial cells and prototissues, endowing artificial cells with tuneable mechanical properties, programmable environmental responsiveness and precise targeted delivery capabilities. Unlike traditional cancer diagnostic and therapeutic agents that suffer from poor tumour specificity, rapid systemic clearance and severe off-target effects, artificial cells leverage their biomimetic design to achieve prolonged circulatory retention, precise tumour site accumulation, and controlled release of diagnostic probes and therapeutic payloads. This review systematically explores the major types of artificial cells, modular bottom-up construction methods, and advanced biomimetic behaviours of artificial cell systems. Additionally, it highlights their cutting-edge applications in integrated cancer theranostics, including tumour biomarker sensing, targeted drug delivery, and immunomodulatory therapy. Finally, the review addresses key challenges and future directions to accelerate their clinical translation in oncology.</p>","PeriodicalId":100686,"journal":{"name":"Interdisciplinary Medicine","volume":"4 4","pages":""},"PeriodicalIF":13.6,"publicationDate":"2026-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/inmd.70139","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148522755","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}