BIOMATERIALS生物材料
BIOMATERIALS(英文缩写 BIOMATERIALS),ISSN 0142-9612,eISSN 1878-5905,中文译名:生物材料 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-11-01 至 2026-10-31，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 15.304 | Q1 |
| 2022 | 14.000 | Q1 |
| 2023 | 12.800 | Q1 |
| 2024 | 12.900 | Q1 |
| 2025 | 13.600 | Q1 |
BIOMATERIALS 最新收录文献
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1. Rapid microwave-assisted synthesis of ZnMn dual-atom nanozymes for cancer catalytic immunotherapy.
1. 微波辅助快速合成ZnMn双原子纳米酶用于癌症催化免疫治疗PMID:日期:2026-09-30Catalytic nanomedicines face a persistent trade-off between structurally defined active sites and rapid synthesis. A microwave-assisted salt-flux conversion is developed that transforms a bimetallic metal-organic framework precursor within 3 min into nitrogen-doped carbon-supported ZnMn dual-atom nanozymes (ZnMn DAzymes). Aberration-corrected HAADF-STEM and dual-edge X-ray absorption fine structure analyses support adjacent Zn-Mn sites with an N-dominated ZnMn-N-like coordination motif. Steady-state kinetics and density functional theory calculations suggest cooperative catalysis: Zn modulates HO adsorption and O-O bond activation, whereas Mn provides stronger HO chemisorption and redox flexibility, jointly enhancing catalase-, peroxidase-, and oxidase-like activities. The resulting cascade decomposes HO, relieves hypoxia, generates reactive oxygen species, and depletes glutathione, inducing mitochondrial dysfunction, immunogenic cell death, cGAS-STING-associated signaling, dendritic-cell maturation, and effector T-cell infiltration. Glutathione-responsive Mn release additionally enables activatable T-weighted magnetic resonance contrast. Combined with αPD-L1, ZnMn DAzymes suppress primary and distal tumors by approximately 90%, reduce lung metastases by 92%, and prolong survival in 4T1 models. This work provides a rapid route to ZnMn dual-atom nanozymes for catalytic immunotherapy.
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2. Near-infrared photocatalytic oral microalgae-carbon nitride-based nanozyme ameliorate Parkinson's disease via suppressing gut microbiota-indole-3-lactic acid-brain axis-mediated neuroinflammation.
2. 近红外光催化口服微藻-氮化碳基纳米酶通过抑制肠道菌群-吲哚-3-乳酸-脑轴介导的神经炎症改善帕金森病PMID:日期:2026-09-30Gut microbiota modulates gut-brain crosstalk in Parkinson's disease (PD), yet effective therapies are still lacking. Herein, we report an orally administrable microalgae-nanozyme platform (SP@SKCN) via combining sulfur/potassium (S/K) co-doped carbon nitride (SKCN) with Spirulina platensis (SP), offering a novel therapeutic strategy for PD. Uniform S-K co-doping significantly narrows the bandgap of carbon nitride (2.2 eV), endowing SKCN with high near-infrared (NIR)-photocatalytic activity and a star-shaped network morphology, realizing NIR-driven water splitting for H/O generation. Meanwhile, SKCN exhibits superoxide dismutase (SOD)/catalase (CAT) mimetic enzyme activities, efficiently scavenging reactive oxygen species (ROS) and synergistically alleviating inflammation. SP incorporation protects SP@SKCN from gastric acid degradation, prolongs its intestinal retention time, and mediates sustained SKCN release. Notably, SP@SKCN remarkedly improves motor deficits, gastrointestinal dysfunctions, and dopaminergic neuron loss in PD mice. 16 S rRNA sequencing and targeted metabolomics reveal that SP@SKCN treatment reverses both PD-associated microbiota changes and the MPTP-induced reduction in indole-3-lactic acid (ILA). Further experiments indicate that SP@SKCN alleviate intestinal inflammation and gut barrier disruption, consequently attenuating systemic inflammation. Mechanistically, SP@SKCN restore the ILA/aryl hydrocarbon receptor (AHR)/NF-κB signaling caused by disturbed gut microbiota mediated the glial cells activation, which eventually reduce dopaminergic neuron death. Collectively, SP@SKCN ameliorates PD via regulating the microbiota-ILA-brain axis.
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3. Engineering extracellular vesicles for multi-cargo co-delivery in silicosis and related fibrotic diseases: design strategies and translational prospects.
3. 工程化细胞外囊泡用于矽肺及相关纤维化疾病中的多货物共递送：设计策略与转化前景PMID:日期:2026-09-30Silicosis remains therapeutically intractable because its three driver axes-the NLRP3 inflammasome, ROS/Nrf2 oxidative stress, and TGF-β/Smad fibrosis-interlock into a self-reinforcing network whose topological redundancy reroutes signalling around any single-target drug, the structural basis for repeated single-agent failure. Existing nanocarriers cannot meet the resulting demand for multi-cargo delivery: lipid nanoparticles risk triggering NLRP3, polymeric carriers escape endosomes too poorly to deliver nucleic acids, and inorganic particles intensify the ROS-driven fibrotic loop. Engineered exosomes close this gap. Their native architecture matches the silicotic microenvironment and can carry nucleic acids, proteins, and small molecules together at defined ratios across the vesicle population, while surface CD47 can confer immune evasion, donor-encoded integrins can direct cell-selective pulmonary tropism, and membrane fusion can deliver payloads directly into the cytoplasm, - properties we argue must be demonstrated for each engineered construct rather than assumed. Here, we evaluate the complete engineering pipeline - donor-cell selection, GMP-compatible isolation, cargo loading by electroporation and bio-orthogonal surface click chemistry, and stimuli-responsive release whose triggering thresholds have been established in oncological rather than fibrotic settings and require validation in silicosis. Preclinical evidence, graded by a three-tier scheme, is consistent with coordinated multi-axis efficacy spanning NLRP3 suppression, Nrf2 restoration, and TGF-β/Smad blockade, but remains predominantly Grade B and C; we critically appraise manufacturing scalability, co-loading optimization, and endotype-matched dosing as the milestones still separating this platform from clinical deployment.
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4. Fluoropharmacology: intrinsic AIE antibiotics as theranostic photosensitizers against resistance and systemic toxicity.
4. 荧光药理学：本征AIE抗生素作为诊疗一体化光敏剂对抗耐药性与全身毒性PMID:日期:2026-09-27Fluoropharmacology integrates pharmacokinetics/pharmacodynamics with real-time visualization by employing intrinsically fluorescent drugs that combine therapy and luminescence in a single entity. Herein, we report the systematic characterization that clinically approved quinolone antibiotics exhibit intrinsic aggregation-induced emission (AIE) characteristics. Mechanistic studies reveal that the AIE behavior originates from restricted intramolecular motion, thereby establishing the "drug-probe unity" principle that a single molecular architecture inherently encodes pharmacological activity, fluorescence emission, and photosensitizing capability. Exploiting this intrinsic property, we strategically repurpose the historically problematic phototoxicity of quinolones into a theranostic advantage by developing them as photosensitizers for localized antimicrobial therapy. This approach enables visualized pharmacokinetics/pharmacodynamics, synergistic antibacterial efficacy combining intrinsic antibiotic action with photodynamic effects against resistance and systemic toxicity through confined topical application. Beyond elucidating the AIE mechanisms of quinolones, this work proposes Fluoropharmacology as a promising framework that could potentially reshape drug discovery and utilization. By revealing that countless existing and future fluorescent drugs possess untapped visualization capabilities, Fluoropharmacology transforms conventional pharmacopeia into intelligent, image-guided theranostic agents, enabling observation of molecular events within living systems, illuminating the once-invisible journey of drugs from administration to action, and ultimately advancing personalized precision medicine that safeguards human health, where every fluorescent molecule narrates its own healing story.
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5. Spatially compartmentalized fibrotic tumor microtissues via embedded coaxial 3D bioprinting for enhanced barrier function and drug resistance.
PMID:日期:2026-09-26Fibrosis is a prominent feature of the tumor microenvironment (TME) that contributes to tumor progression and therapeutic resistance. Here, we developed an embedded coaxial 3D bioprinting strategy to fabricate spatially compartmentalized fibrotic tumor microtissues with controlled tumor-stromal organization. Compared with mixed spheroids, coaxial spheroids exhibited enhanced hypoxia, fibroblast activation, and ECM deposition, together with reduced drug penetration and increased therapeutic resistance. These responses were supported by molecular and functional analyses. Collectively, our findings show that controlled tumor-stromal organization is closely associated with fibrosis- and hypoxia-related drug resistance. The embedded coaxial bioprinting approach provides a reproducible and tunable engineering framework for systematically investigating how controlled variations in tumor-core diameter, stromal-shell thickness, and cellular positioning influence fibrotic tumor phenotypes and therapeutic responses in vitro.
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6. From ear to eye: Transparent alkali-treated autologous cartilage for corneal stromal regeneration.
6. 从耳到眼：用于角膜基质再生的透明碱处理自体软骨PMID:日期:2026-09-24Corneal blindness represents a major global health burden, with donor shortage and immune rejection remaining significant challenges in transplantation therapy. Here, we present an innovative approach using autologous auricular cartilage as a sustainable tissue source for corneal regeneration. The resulting 12-h treated grafts achieved 60-70% in vitro transmittance, tensile strength of ∼2 MPa, suture retention of 0.48 N, water content of ∼78%, contact angle of ∼35°, and refractive index of 1.332 - values closely resembling native corneal stroma. In a rabbit lamellar keratoplasty model, these autologous scaffolds promoted rapid re-epithelialization, suppressed myofibroblast activation (α-SMA area reduced by ∼70% versus control, *p* < 0.01), and restored full corneal transparency and stromal architecture within 8 weeks, with significantly lower neovascularization and inflammation than controls. The autologous nature of the grafts prevented immune rejection and supported seamless tissue integration. This work establishes autologous cartilage as a clinically viable biomaterial for corneal reconstruction, offering a practical solution to donor scarcity while eliminating the need for immunosuppression. Our findings demonstrate the great potential of autologous tissue transformation in regenerative ophthalmology.
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7. Inhalable mucus-penetrating and senescence-targeted nanoliposomes reverse senescence to overcome chemoresistance for enhanced lung cancer therapy.
7. 可吸入的黏液穿透型衰老靶向纳米脂质体逆转衰老以克服化疗耐药从而实现增强的肺癌治疗PMID:日期:2026-09-23Lung cancer therapy is severely hindered by the pulmonary mucus barrier and chemotherapy resistance driven by therapy-induced senescence (TIS) following DNA-damaging agents. Herein, we report an inhalable, mucus-penetrating nanoliposomes (DR@DPPC-Apt) engineered by incorporating an L1 cell adhesion molecule (L1CAM)-targeting cholesterol-modified aptamer into dipalmitoyl phosphatidylcholine (DPPC)-based nanoliposomes co-encapsulating rapamycin and doxorubicin. Upon noninvasive inhalation, the nanoliposomes leverage compositional similarity to efficiently traverse the mucus barrier and actively target senescent lung cancer cells via aptamer-mediated recognition of overexpressed L1CAM, achieving enhanced cellular uptake and selective drug accumulation in tumor sites. Intratumorally, rapamycin potently inhibits the mammalian target of rapamycin (mTOR) pathway to reverse the senescent phenotype, which in turn enhances drug retention, hyperactivates autophagy, and blocks senescence propagation, thereby resensitizing cancer cells to chemotherapy and overcoming acquired resistance. In a chemoresistant lung cancer mouse model, inhalation of DR@DPPC-Apt significantly suppresses tumor growth without appreciable systemic toxicity. This strategy establishes a highly effective therapeutic paradigm for chemoresistant lung cancer by integrating senescence-targeted delivery with pharmacological senescence reversal, thereby offering a promising clinically translatable approach for enhanced lung cancer therapy.
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8. Geogrid-inspired robust mineralized coating promotes vascularized osseointegration of polyetheretherketone.
8. 土工格栅启发的坚固矿化涂层促进聚醚醚酮的血管化骨整合PMID:日期:2026-09-23Polyetheretherketone (PEEK) is widely used in orthopedic implants but integrates poorly with surrounding bone. Bioactive coatings can improve this, yet most adhere weakly to PEEK's inert surface-causing delamination and inflammation. Inspired by geogrid structures used in highway pavement engineering, this study presents a novel strategy for fabricating a robust strontium (Sr)-doped hydroxyapatite coating on the PEEK surface through structural mimicry. First, a porous adhesive intermediate layer resembling geogrid architecture is created on the PEEK surface via sulfonation combined with polydopamine modification. Subsequently, the modified substrate is immersed in Sr-supplemented simulated body fluid to promote ion adsorption and induce mineralization. The resulting mineralized coating achieves strong interfacial bonding with the intermediate layer via mechanical interlocking and chemical/physical interactions, thereby substantially enhancing its stability under physiological loading conditions. Both in vitro and in vivo evaluations demonstrate that the Sr-doped mineralized coating endows PEEK with superior vascularization and osteoinductive properties. In conclusion, this study proposes an innovative and effective strategy for constructing a durable bioactive coating on PEEK surfaces, holding significant promise for advancing its clinical efficacy in orthopedic applications.
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9. Neutrophil membrane-camouflaged ruthenium single-atom nanozymes precisely eliminate neutrophil extracellular traps to reprogram redox-immune microenvironment in intracerebral hemorrhage.
9. 中性粒细胞膜伪装的钌单原子纳米酶精准消除中性粒细胞胞外诱捕网以重编程脑出血中的氧化还原免疫微环境PMID:日期:2026-09-23Intracerebral hemorrhage (ICH) causes severe secondary brain injury driven by excessive reactive oxygen species (ROS) deposition, neutrophil extracellular traps (NETs) formation, and persistent neuroinflammation. The pathological peptidylarginine deiminase 4 (PAD4)-mediated NETosis and aberrant crosstalk between pro-inflammatory neutrophils and M1-polarized microglia collectively therapeutic strategies remain lacking. Herein, we fabricate a bone marrow-derived neutrophils membrane-camouflaged ruthenium single-atom nanozyme (Ru-SAN) loaded with the PAD4 inhibitor GSK484 (Ru-SAN/G@M) for precise ICH treatment. Taking advantage of neutrophil-derived inflammatory homing properties, Ru-SAN/G@M efficiently crosses the blood brain barrier and specifically accumulates at neuroinflammatory lesions. The Ru single-atom sites exert excellent antioxidant enzyme-mimetic activity to eliminate excess ROS, while encapsulated GSK484 inhibits PAD4 activation and blocks pathological NET formation. This dual modulation disrupts detrimental neutrophil-microglia inflammatory communication, reverses microglial M1 polarization toward the protective M2 phenotype, and alleviates neuronal apoptosis and secondary brain damage. This study develops an integrated catalytic and pharmacological strategy to remodel the redox-immune microenvironment, providing a promising therapeutic paradigm for ICH and other ROS-related neuroinflammatory disorders.
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10. Antitumor immunotherapeutic nanoagents enable molecular-photoswitching-based dynamic regulation of enzymatic activity of IDO1 for blocking immune evasion.
PMID:日期:2026-09-23We have fabricated a new type of MOFs-based nanoagent (SP@POMU-A) capable of suppressing tumor progression and metastasis by blocking immune evasion based on the molecular-photoswitching-enabled dynamic regulation of the enzymatic activity of IDO1. SP@POMU-A undergoes site-specific disintegration in lysosomes and releases the photosensitizer porphyrin, biometallic ion Mg, and molecular photoswitch spiropyran (SP), with them playing distinct roles in enabling immunotherapy via a highly synergistic manner. Porphyrin and Mg synergistically prime the adaptive antitumor immune response based on the photosensitization ability of the former and adjuvant-like activity of the latter, respectively. SP upon phototriggering isomerizes to merocyanine with the latter capable of inactivating IDO1 and therefore blocking its role in tumor immune evasion. Thus, SP@POMU-A upon phototriggering can boost antitumor immunity and simultaneously block immune evasion, eventually potently inhibiting the tumor progression. The ability of SP@POMU-A to confer immunological memory for mounting a specific immune response upon re-exposure to the invasion of tumor cells has also been verified in an in vivo tumor model featured with typical pathological characteristics regarding immunosuppressive tumor microenvironment (TME). This proof-of-concept implementation opens a way to optically manipulate the enzymatic activity to relieve the immunosuppressive TME for synergistic antitumor with enhanced precision and efficacy.