Biomaterials research最新文献

{"title":"Erratum to \"Amino Acid Metabolism-Regulated Nanomedicine for Enhanced Tumor Immunotherapy through Synergistic Regulation of Immune Microenvironment\".","authors":"Xiuying Duan, Yilei Zhao, Houyang Hu, Xuechun Wang, Jie Yan, Songyan Li, Yueying Zhang, Jianwei Jiao, Guiqiang Zhang","doi":"10.34133/bmr.0352","DOIUrl":"10.34133/bmr.0352","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.34133/bmr.0048.].</p>","PeriodicalId":93902,"journal":{"name":"Biomaterials research","volume":"30 ","pages":"0352"},"PeriodicalIF":9.8,"publicationDate":"2026-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13096678/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147792109","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":"Focused Ultrasound-Triggered Burst Release and Enrichment of Engineered Bacteria for Tumor Therapy.","authors":"Jinhee Yoo, Yunhee Hwang, Mihyeon Park, Honghyeon Ha, Myeong Ryeol Choi, Sung In Lim, Byullee Park, Yong Joo Ahn, Won Jong Kim, Gyoo Yeol Jung, Hyung Ham Kim","doi":"10.34133/bmr.0354","DOIUrl":"10.34133/bmr.0354","url":null,"abstract":"<p><p>Ultrasound has been widely used in bacteria-based tumor therapy for targeted drug delivery due to its noninvasive ability to control bacteria. However, current approaches achieve only gradual release of therapeutic agents and rely on limited natural homing ability, resulting in poor treatment efficacy. Here, we demonstrate that focused ultrasound (FUS) can simultaneously induce burst release within tumors and local enrichment of therapeutics, enhancing precise and controllable spatiotemporal drug delivery efficiency within tumor microenvironments in living-therapeutic biomaterial system. We achieved FUS-triggered bacterial burst release by coexpressing gas vesicles (GVs), protein nanostructures that induce cavitation, and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), which increases antitumor efficacy. Furthermore, we show that FUS enhances enrichment of therapeutics at the tumor site by manipulating bacteria toward tumor vessel walls and increasing tumor permeability via sonopermeation. In a mouse model, we demonstrated clinical potential by achieving a 40% reduction in tumor volume using probiotic <i>Escherichia coli</i> Nissle (EcN) 1917 with a short 2-min FUS exposure and no exogenous agents. This work shows that physical ultrasound control provides an intuitive, highly efficient, and easily applicable biohybrid approach to bacteria-based tumor therapy, offering a simple and widely accessible strategy that can be broadly adapted to diverse living biomaterial systems.</p>","PeriodicalId":93902,"journal":{"name":"Biomaterials research","volume":"30 ","pages":"0354"},"PeriodicalIF":9.8,"publicationDate":"2026-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13084060/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147724959","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":"Nanoparticle-Loaded Injectable Hydrogel Alleviates Titanium Particle-Induced Osteolysis by Disrupting GATA6/DDX3X-Mediated Macrophage Inflammation.","authors":"Sipeng Lin, Taihe Liu, Qi Zhu, Zhuji Ouyang, Yifan Yu, Haopeng Sun, Changchuan Li, Shixun Li, Chenhao Pan, Wing Cheuk Ko, Haoxian Liu, Jin Liu, Shuangxing Li, Jinchang Chen, Shaojian Wu, Jichao Ye, Liangbin Gao, Yue Ding","doi":"10.34133/bmr.0353","DOIUrl":"10.34133/bmr.0353","url":null,"abstract":"<p><p>Aseptic loosening (AL) represents the primary cause of joint arthroplasty failure, which is predominantly triggered by chronic inflammatory reactions to prosthetic wear particles, with macrophages serving as the central effector cells. Accumulating evidence indicates that the crosstalk between endoplasmic reticulum stress and mitochondrial stress exacerbates macrophage-mediated inflammation; however, the core molecular regulators orchestrating this pathological cascade remain elusive. Herein, we investigated the functional role of the GATA6/DDX3X (DEAD-box helicase 3 X-linked) axis in titanium particle (TiP)-induced macrophage inflammatory responses and further explored the therapeutic potential of nanoparticle-loaded injectable hydrogels for AL. Specifically, a si-DDX3X-loaded nanoparticle hydrogel (si-DDX3X NPs@Hy) was fabricated and characterized, and its therapeutic efficacy was evaluated in vivo. Our results demonstrated that DDX3X expression was significantly up-regulated in both TiP-stimulated bone marrow-derived macrophages and periprosthetic tissues obtained from AL patients. Functional assays revealed that DDX3X promoted mitochondria-endoplasmic reticulum interplay, which in turn facilitated NLRP3 inflammasome assembly and subsequent interleukin-1β secretion. Mechanistically, GATA6 directly bound to the transcription start site of the DDX3X gene, thereby suppressing its transcriptional expression and abrogating DDX3X-mediated proinflammatory effects. The synthesized si-DDX3X NPs@Hy exhibited favorable physicochemical properties; local administration of this hydrogel markedly attenuated TiP-induced calvarial osteolysis in mice, accompanied by reduced osteoclastogenesis, proinflammatory cytokine production, and M1 macrophage polarization in the lesion microenvironment. Collectively, this study identifies the GATA6/DDX3X axis as a pivotal regulator of TiP-driven macrophage inflammation and validates the si-DDX3X NPs@Hy as a promising therapeutic strategy for targeting wear particle-induced inflammation, which holds great potential for improving the long-term prognosis of joint arthroplasty.</p>","PeriodicalId":93902,"journal":{"name":"Biomaterials research","volume":"30 ","pages":"0353"},"PeriodicalIF":9.8,"publicationDate":"2026-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13084059/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147724994","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":"Autophagy-Modulated Sonodynamic Therapy Triggers Mitochondrial Catastrophe for Potent Immunogenic Tumor Eradication.","authors":"Mengmeng Li, Hua Song, Ya Zhu, Wei Zhang, Tian'an Jiang","doi":"10.34133/bmr.0348","DOIUrl":"10.34133/bmr.0348","url":null,"abstract":"<p><p>Sonodynamic immunotherapy represents a promising strategy for cervical cancer treatment by stimulating antitumor immune responses. However, therapy-induced prosurvival autophagy may attenuate therapeutic efficacy. To address this limitation, we constructed multifunctional nanoparticles (poly[lactic-<i>co</i>-glycolic acid]-b-poly[ethylene glycol] [PLGA-PEG_2,000]-based nanoparticles coloaded with hematoporphyrin monomethyl ether and SAR405 [PHS NPs]) codelivering the sonosensitizer hematoporphyrin monomethyl ether and the selective vacuolar protein sorting 34 inhibitor SAR405. Upon low-intensity focused ultrasound irradiation, PHS NPs generated reactive oxygen species that induced mitochondrial stress while concurrently modulating autophagic flux through VPS34 inhibition. This coordinated intervention was associated with microtubule-associated protein 1A/1B-light chain 3-II and p62 coaccumulation and the presence of undegraded autolysosomal structures, suggesting impairment of lysosome-associated autophagic degradation. Enhanced oxidative stress, together with modulation of autophagic flux, was accompanied by lysosomal dysfunction and reduced degradative capacity. These alterations were associated with sustained intracellular stress and amplified oxidative injury in tumor cells. Functionally, the combined treatment suppressed tumor growth, promoted immunogenic cell death, and was accompanied by macrophage polarization toward an M1-like phenotype and increased CD8⁺ T cell infiltration. Validated in HPV-associated tumor models, this nanoparticle-based strategy provides a rational and potentially translatable platform to mitigate autophagy-associated adaptive responses and enhance the therapeutic potential of sonodynamic immunotherapy in solid tumors.</p>","PeriodicalId":93902,"journal":{"name":"Biomaterials research","volume":"30 ","pages":"0348"},"PeriodicalIF":9.8,"publicationDate":"2026-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13081276/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147701140","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":"Fast-Dissolving Sodium Alginate-Based Microneedle Patch Integrating Tranilast and Glabridin-Loaded Nanoparticles for Dual-Action Hypertrophic Scar Therapy.","authors":"Ayesha Younas, Muhammad Sohail, Yueting Li, Quan Zhou, Yonghui Shen, Shuanghu Wang, Yaru Shi, Zhenqiu Shang, Chuxiao Shao, Jian Xiao","doi":"10.34133/bmr.0351","DOIUrl":"10.34133/bmr.0351","url":null,"abstract":"<p><p>Hypertrophic scars (HSs) are a prevalent skin condition that imposes substantial functional, financial, and aesthetic burdens, with existing treatments often leading to recurrence, pain, and adverse effects. To address these issues, we propose a first-in-class fast-dissolving sodium alginate-based microneedle patch (sMN) that achieves sequential, dual-release kinetics by integrating tranilast (TS) and glabridin (GL)-loaded nanoparticles (GLNPs), termed TS+GLNPs@sMN. Our system uniquely integrates rapid TS release for immediate \"OFF\" switching, suppression of fibroblast activation, stabilization of mast cells, and relief of pruritus, with sustained GL release from GLNPs for prolonged \"ON\" switching, which promotes fibroblast apoptosis and modulates scar matrix deposition. This sequential \"OFF-to-ON\" paradigm mirrors the temporal progression of HS pathophysiology, with early inflammatory events preceding fibrotic remodeling. The cone-shaped microneedle patch (~565 μm) demonstrated efficient skin penetration/recovery, even drug distribution, fast dissolution (180 ± 20 s), high loading capacity, and desirable release kinetics. In vitro evaluations confirmed promising anti-proliferative, anti-migratory, and anti-angiogenic effects. Preliminary in vivo biocompatibility in mice was satisfactory, with no skin irritation and normal complete blood count, renal, and hepatic function. In vivo studies in a rabbit ear HS model demonstrate accelerated HS healing, reduced HS thickness, epidermal thickness index (ETI), scar elevation index (SEI), and collagen deposition, along with decreased profibrotic markers, inflammatory cytokines, and angiogenic factors. Overall, the TS+GLNPs@sMN patch offers a minimally invasive, self-administrable, dual-action therapeutic strategy for enhanced HS management, with safety and efficacy in preclinical models.</p>","PeriodicalId":93902,"journal":{"name":"Biomaterials research","volume":"30 ","pages":"0351"},"PeriodicalIF":9.8,"publicationDate":"2026-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13074273/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147694411","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":"Biomaterials Based on Bacteria for Cancer Clinical Therapy.","authors":"Chongyu Liang, Xiaoming Sun, Lingyu Xin, Meiting Yi, Kai Ma, Zicun Li, Hao Ran, Wei Zhu, Zenghao Wang, Jiandong Zhang","doi":"10.34133/bmr.0350","DOIUrl":"10.34133/bmr.0350","url":null,"abstract":"<p><p>Cancer remains a major global health burden, necessitating innovative therapies. Bacterial therapy has reemerged as a transformative strategy, particularly for the potential to overcome resistance to conventional treatments. Bacteria could selectively colonize the hypoxic, acidic, and immunosuppressive tumor microenvironment. Besides, synthetic biology has enabled these bacteria to be engineered into precise living therapeutics, capable of localized drug delivery, targeted immune modulation, and remodeling of the tumor microenvironment. This review systematically explores the mechanisms by which engineered bacteria exert antitumor effects, including direct oncolysis, immunogenic cell death, and reversal of immunosuppression. Furthermore, the synergistic potential of bacterial therapy with standard therapies is discussed. Bacteria can sensitize tumors to chemotherapy through prodrug activation or reverse microbiota-mediated chemoresistance. In radiotherapy, bacteria could act as radiosensitizers and radioprotectors while amplifying abscopal effects. Combined with immunotherapy, they effectively convert immunologically \"cold\" tumors into \"hot\" ones, enhancing the application of immune checkpoint inhibitors. The role of the gut microbiota in shaping systemic antitumor immunity is also discussed. Finally, the article critically assesses the clinical translation landscape, examining representative strains in development, addressing safety and manufacturing challenges, and highlighting future directions. This review aims to provide a foundational perspective for developing safer and more effective bacterially mediated anticancer strategies.</p>","PeriodicalId":93902,"journal":{"name":"Biomaterials research","volume":"30 ","pages":"0350"},"PeriodicalIF":9.8,"publicationDate":"2026-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13074759/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147694339","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":"Fibroblast Activation Protein Alpha-Targeted Nanoparticles for Tumor Microenvironment Remodeling and Antitumor Therapy in Triple-Negative Breast Cancer.","authors":"Ana Lameirinhas, Paula Díez, Francisco J Hicke, Anna Ágreda-Roca, Sandra Torres-Ruiz, Paloma Sánchez-Serrano, Marta Tapia, Ana Lluch, Begoña Bermejo, Juan Miguel Cejalvo, Ramón Martínez-Máñez, Pilar Eroles, Iris Garrido-Cano","doi":"10.34133/bmr.0347","DOIUrl":"10.34133/bmr.0347","url":null,"abstract":"<p><p>Triple-negative breast cancer (TNBC) remains a highly aggressive subtype with limited treatment options and poor prognosis. While most therapies target tumor cells, the tumor microenvironment (TME), particularly cancer-associated fibroblasts (CAFs), plays a key role in tumor progression, therapy resistance, and immune suppression. We developed NP-FAP-DOX, a mesoporous silica nanoparticle-based nanodevice loaded with doxorubicin and functionalized with a fibroblast activation protein alpha (FAP-α) ligand peptide for selective binding to FAP-α-positive CAFs. FAP-α targeting ability and cytotoxic effect were assessed in TNBC cells, patient-derived CAFs, and patient-derived organoids (PDOs). In vivo efficacy was evaluated in the murine orthotopic TNBC 4T1 allograft model, assessing tumor growth inhibition, toxicity, CAFs depletion, extracellular matrix degradation, apoptosis induction, and TME-associated cellular and stromal changes. NP-FAP-DOX exhibited controlled drug release, selective binding to FAP-α, and cytotoxicity in TNBC cells, patient-derived CAFs, and PDOs. In vivo, NP-FAP-DOX reduced tumor growth, depleted CAFs, degraded the extracellular matrix, induced apoptosis, increased lymphocyte infiltration, and decreased M2-like macrophages. Compared with free doxorubicin, NP-FAP-DOX enhanced therapeutic efficacy while reducing cardiotoxicity and systemic side effects. These findings highlight NP-FAP-DOX as a promising nanomedicine strategy for TNBC, integrating tumor inhibition, TME remodeling, and immune activation, with strong potential for clinical translation.</p>","PeriodicalId":93902,"journal":{"name":"Biomaterials research","volume":"30 ","pages":"0347"},"PeriodicalIF":9.8,"publicationDate":"2026-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13058225/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147647806","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":"Boosting Boron Neutron Capture Therapy through Ferroptosis Activation with a Biomimetic Nanoenhancer.","authors":"Jiayi Wang, Linwen Lv, Hao Li, Xin Pan, Junhui Zhang, Jiaxuan Li, Ruyu Yan, Jiaxin Wan, Haojun Liang, Bingbing Peng, Mingxin Yang, Yanan Chang, Juan Li, Hui Yuan, Minghua Shen, Gengmei Xing, Kui Chen","doi":"10.34133/bmr.0343","DOIUrl":"10.34133/bmr.0343","url":null,"abstract":"<p><p>Boron neutron capture therapy (BNCT) is an emerging tumor radiotherapeutic modality, but its efficacy is limited by incomplete understanding of tumor cell death mechanisms. Here, we demonstrate that BNCT fails to sufficiently induce ferroptosis-a form of programmed cell death with important implications for both tumor elimination and immune activation-which constrains its therapeutic potential. Using proteomic profiling across multiple tumor cell lines, we found that although BN-triggered mitochondrial dysfunction activated several death-related pathways, robust ferroptosis was not achieved. To address this, we developed a biomimetic nanoagent, m(E@BN), composed of erastin-loaded boron nitride nanosheets coated with tumor cell membranes for targeted delivery. This system significantly enhanced BNCT-induced ferroptosis in vitro and in vivo, synergistically promoting lipid peroxidation and iron metabolism dysregulation without aggravating DNA injury. Furthermore, m(E@BN)-augmented BNCT stimulated potent antitumor immunity, evidenced by increased T cell infiltration and establishment of immune memory. Our study not only elucidates a mechanistic limitation of BNCT but also offers an effective nanomedicine-based strategy to amplify its efficacy through ferroptosis activation, providing a broadly applicable paradigm for improving radiotherapeutic outcomes.</p>","PeriodicalId":93902,"journal":{"name":"Biomaterials research","volume":"30 ","pages":"0343"},"PeriodicalIF":9.8,"publicationDate":"2026-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13047272/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147625090","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":"A Needlelike Nano-hydroxyapatite-Based Hydrogel Accelerates Critical Bone Defect Regeneration via Osteo-/Angiogenesis and Osteoimmune Regulation.","authors":"Dingli Xu, Leidong Lian, Zhe Luo, Yanxue Dong, Chaonan He, Minghui Chu, Liangjie Lu, Weihu Ma, Kaifeng Gan","doi":"10.34133/bmr.0344","DOIUrl":"10.34133/bmr.0344","url":null,"abstract":"<p><p>The management of critical-sized bone defects has attracted heightened interest due to its challenging nature. To date, numerous engineered tissues incorporating nano-hydroxyapatite (nHap) have been proposed; however, nHap continues to encounter limitations, particularly regarding its inadequate immunomodulatory effects on bone. Therefore, needlelike nHap (NnHap)-based scaffolds were fabricated using a polylactic acid derivative and carboxymethyl chitosan. We hypothesize that NnHap@CP can not only promote bone immunomodulatory effects and angiogenesis in human umbilical vein endothelial cells through M2 subtype polarization but also directly promote osteogenesis in rat bone-marrow-derived mesenchymal stem cells (rBMSCs). Furthermore, mass spectrometry was employed to determine that osteoprotegerin/RANK/RANKL may represent a potential signaling pathway through which NnHap@CP enhances the osteogenesis of rBMSCs. In our study, NnHap@CP demonstrated a satisfactory effect on M2 subtype polarization in macrophages and enhanced osteogenesis in rBMSCs, as observed in an in vitro study. We employed NnHap@CP for the in vivo examination of a rat model with cranial critical-sized bone defects. We discovered that NnHap@CP significantly enhances new bone regeneration and neovascularization, potentially serving as an innovative treatment strategy for critical bone defects.</p>","PeriodicalId":93902,"journal":{"name":"Biomaterials research","volume":"30 ","pages":"0344"},"PeriodicalIF":9.8,"publicationDate":"2026-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13044407/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147625007","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":"Uremic Clearance Granules Regulate Immune Equilibrium via Gut Microbiome to Alleviate Chronic Renal Failure.","authors":"Qian Huang, Zhuowen Liang, Yuqing Cui, Jianxin Diao, Tianshu Zhou, Lei Shi, Zhixin Deng, Rushang Wang, Haitao Yuan, Kun Chen, Ying Du, Ali Chen, Jiayun Chen, Wei Xiao","doi":"10.34133/bmr.0342","DOIUrl":"10.34133/bmr.0342","url":null,"abstract":"<p><p>Chronic renal failure (CRF) is the common end point of various chronic kidney diseases, and there is currently no specific drug for CRF. Effectively halting its progression remains a clinical challenge. Gut microbiota disorders are a key factor influencing immune dysfunction in chronic kidney disease patients. Intervening in gut microbiota to improve immune regulatory function in patients could serve as a new strategy for treating CRF with Traditional Chinese Medicine. Uremic Clearance Granules (UCG), a Traditional Chinese Medicine formulation, effectively attenuate CRF progression, but their active components and mechanisms remain undefined. This study investigates how UCG mitigate CRF via coordinated regulation of gut microbiota, metabolites, and the T helper 17 cells / regulatory T cell axis. Using an adenine-induced CRF mouse model, we combined gut microbiota depletion, fecal microbiota transplantation, 16<i>S</i> rRNA sequencing, and metabolomics to delineate the gut-kidney interactions underlying UCG efficacy. Flow cytometry quantified immune cell profiles in blood, and microbial intervention experiments verified the therapeutic role of <i>Bifidobacterium animalis</i> (<i>B. animalis</i>). In this study, we found that UCG treatment alleviated renal injury, reduced intestinal permeability, and up-regulated intestinal barrier markers. Microbiota depletion and fecal microbiota transplantation demonstrated that UCG's renoprotective effects depend on gut microbial modulation. Specifically, UCG ameliorates CRF through gut-kidney axis remodeling by enhancing <i>B. animalis</i> abundance and sophocarpine, thereby rebalancing T helper 17/regulatory T immunity and preserving renal function. These findings identify a microbiota-dependent immunometabolic mechanism for UCG and highlight a potential therapeutic strategy for CRF via the drug-microbiota axis.</p>","PeriodicalId":93902,"journal":{"name":"Biomaterials research","volume":"30 ","pages":"0342"},"PeriodicalIF":9.8,"publicationDate":"2026-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13033834/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147596766","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}