Materials Today Bio最新文献_第2页

Colloid-patterned surfaces distinguish malignant mechanophenotypes 胶体图案表面区分恶性机械表型

IF 10.2 1区医学 Q1 ENGINEERING, BIOMEDICAL

Materials Today Bio

Pub Date : 2026-04-01 Epub Date: 2026-01-19 DOI: 10.1016/j.mtbio.2026.102800

Chalom Zemmour , Mor Ozeri , Ora T. Cohen , Eduard Berenshtein , Zakhariya Manevitch , Yael Feinstein-Rotkopf , Irit Rosenhek-Goldian , Hadar Benyamini , Victor Shelukhin , Ofra Benny

Accurate and rapid identification of aggressive cancer cells remains a major clinical challenge. Here, we present a simple, label-free mechanophenotyping platform that integrates controlled colloidal topographies with particle-uptake measurements to reveal biophysical traits associated with metastatic progression. Non-close-packed polystyrene bead arrays were formed on cell culture plates by controlled deposition and stabilized with a thin silicon oxide coating. These arrays display micro- and nano-features with a size range of 0.23–2.3 μm at diverse densities and were used to assess adhesion across cancer cells exhibiting different levels of malignancy. Particle uptake differences were most pronounced for particle diameters above 0.5 μm, whereas adhesion differences emerged predominantly on particles ≥0.7 μm and increased progressively with larger particle sizes. Colloidal topographies were fabricated at particle deposition concentrations of 500 μg/mL and 1000 μg/mL, and adhesion differences were observed under both conditions, with more potent effects at the higher concentration. At the metastatic site, cells exhibited increased particle uptake, stronger adhesion, and a larger morphological engagement on colloid-coated substrates, characterized by extensive actin-rich protrusions wrapping individual particles. AFM force mapping confirmed higher adhesion forces to a colloidal probe, while transcriptomic profiling revealed enrichment of adhesion and ECM-remodeling pathways in the adhesive metastatic state. We also find that lymphatically selected cells exhibit reduced adhesion on colloid-coated surfaces but higher particle uptake compared to the primary tumor cells. These results indicate that after leaving the primary tumor, metastatic cells have reduced adhesive potential, which is only regained upon reaching secondary sites. By exposing adhesion differences that are undetectable on flat substrates and linking them to particle uptake assays, this platform produces functional signatures of metastatic potential. This method is technically accessible, compatible with imaging and molecular workflows, and adaptable for high-throughput or clinical analysis, offering a potential route for label-free detection and classification of cancer cells by their aggressiveness.

准确和快速识别侵袭性癌细胞仍然是一个主要的临床挑战。在这里，我们提出了一个简单的、无标记的机械表型平台，该平台整合了受控的胶体地形和颗粒摄取测量，以揭示与转移进展相关的生物物理特征。通过控制沉积在细胞培养板上形成非紧密堆积的聚苯乙烯球阵列，并用薄氧化硅涂层稳定。这些阵列在不同密度下显示尺寸范围为0.23-2.3 μm的微纳米特征，并用于评估不同恶性程度癌细胞之间的粘附性。粒径大于0.5 μm时，吸附差异最为明显；粒径≥0.7 μm时，吸附差异最为明显，且随粒径增大而增大。在颗粒沉积浓度为500 μg/mL和1000 μg/mL的条件下制备胶体形貌，观察到两种条件下的粘附差异，且浓度越高效果越明显。在转移部位，细胞表现出更多的颗粒摄取，更强的粘附性和更大的胶体覆盖底物的形态接合，其特征是广泛的富含肌动蛋白的突起包裹着单个颗粒。AFM力图谱证实胶体探针具有更高的粘附力，而转录组分析显示粘附转移状态中粘附和ecm重塑途径的富集。我们还发现，淋巴选择的细胞在胶体包被表面上的粘附性降低，但与原发肿瘤细胞相比，颗粒摄取更高。这些结果表明，在离开原发肿瘤后，转移细胞的粘附潜力降低，只有在到达继发部位时才能恢复。通过暴露在平面底物上无法检测到的粘附差异，并将其与颗粒摄取测定相连接，该平台产生转移潜力的功能特征。这种方法在技术上是可行的，与成像和分子工作流程兼容，适用于高通量或临床分析，为根据癌细胞的侵袭性进行无标记检测和分类提供了一条潜在的途径。

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引用次数: 0

Multiple-pathway cGAS-STING activation with enhanced mild photothermal therapy through glycolysis regulation for boosting gastric cancer immunotherapy 通过糖酵解调节增强轻度光热治疗的多途径cGAS-STING激活促进胃癌免疫治疗

IF 10.2 1区医学 Q1 ENGINEERING, BIOMEDICAL

Materials Today Bio

Pub Date : 2026-04-01 Epub Date: 2026-01-09 DOI: 10.1016/j.mtbio.2026.102790

Henan Xu , Yuxin Jiang , Ruohao Zhang , Daguang Wang , Jing Feng , Hongjie Zhang

Chemotherapy and photothermal therapy (PTT) have made prominent progress in the treatment of gastric cancer. However, the poor targeting of chemotherapeutic drugs and the thermotolerance or collateral damage induced by PTT lead to suboptimal therapeutic outcomes. To address these issues, we developed a mild PTT (mPTT) nanoparticle based on mesoporous polydopamine (MPDA), loaded with oxaliplatin (OXP) and manganese dioxide (MnO₂), and coated with tumor cell membranes to enhance the targeting capability. On one hand, this nanoparticle disrupts glycolysis by inhibiting hypoxia-inducible factor (HIF), while suppressing heat shock proteins (HSP) to mitigate tumor "thermotolerance". On the other hand, the reactive oxygen species (ROS) generated by the MnO₂-mediated Fenton-like reaction, OXP, and mPTT also induce immunogenic cell death (ICD) to boost adaptive immunity, as well as activate the cGAS-STING pathway through tumor DNA damage to reinforce innate immunity. The activation of both adaptive and innate immune responses triggers a potent antitumor immune reaction, which, combined with chemotherapy and enhanced mPTT, significantly suppresses tumor growth, metastasis and recurrence. This strategy not only enhances the targeting of chemotherapeutic drugs but also provides new possibilities for expanding the field of immunotherapy in gastric cancer by regulating tumor metabolism and enhancing mPTT.

化疗和光热疗法（PTT）在胃癌的治疗中取得了显著进展。然而，化疗药物的靶向性差以及PTT引起的热耐受性或附带损伤导致治疗结果不理想。为了解决这些问题，我们开发了一种基于介孔聚多巴胺（MPDA）的温和PTT （mPTT）纳米颗粒，负载奥沙利铂（OXP）和二氧化锰（MnO2），并包被肿瘤细胞膜以增强靶向能力。一方面，这种纳米颗粒通过抑制缺氧诱导因子（HIF）来破坏糖酵解，同时抑制热休克蛋白（HSP）来减轻肿瘤的“耐热性”。另一方面，mno2介导的Fenton-like反应、OXP和mPTT产生的活性氧（ROS）也诱导免疫原性细胞死亡（ICD）增强适应性免疫，并通过肿瘤DNA损伤激活cGAS-STING通路增强先天免疫。适应性和先天免疫反应的激活触发了一种有效的抗肿瘤免疫反应，这种免疫反应与化疗和增强的mPTT结合，显著抑制肿瘤的生长、转移和复发。该策略不仅增强了化疗药物的靶向性，而且通过调节肿瘤代谢和增强mPTT，为扩大胃癌免疫治疗领域提供了新的可能性。

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引用次数: 0

Biomimetic cancer cell membrane-coated liposomal nanocarriers loaded with silibinin suppress gastric cancer progression via SNHG1/miR-383-5p/HSP90AA1 axis-mediated PI3K/AKT pathway inhibition 装载水飞蓟宾的仿生癌细胞膜包被脂质体纳米载体通过SNHG1/miR-383-5p/HSP90AA1轴介导的PI3K/AKT通路抑制胃癌进展

IF 10.2 1区医学 Q1 ENGINEERING, BIOMEDICAL

Materials Today Bio

Pub Date : 2026-04-01 Epub Date: 2025-12-29 DOI: 10.1016/j.mtbio.2025.102744

Jun Yao , Qiang Sun , Xin Zhang , Dejun Yang , Han Wu, Zunqi Hu, Qing You, Ziran Wei, Weijun Wang

Gastric cancer (GC) remains a major global health problem and demands more effective therapeutic approaches. In this study, we developed a novel biomimetic nanovesicle system—cancer cell membrane-coated liposomal nanocarriers loaded with silibinin (CLip@Sil)—designed for targeted therapy against GC. By integrating network pharmacology with transcriptomic profiling, we identified 13 key target genes, significantly enriched in the PI3K/AKT and IL-17 signaling pathways, with HSP90AA1 emerging as a central regulatory node. Further mechanistic investigation revealed that silibinin exerts its anticancer effect by modulating the SNHG1/miR-383-5p/HSP90AA1 competing endogenous RNA (ceRNA) axis, thereby suppressing the PI3K/AKT pathway. The engineered CLip@Sil system demonstrated enhanced tumor-targeting capacity via its biomimetic cancer-membrane coating, enabling selective drug delivery and accumulation in tumor tissues. In vitro studies confirmed that CLip@Sil inhibited GC cell proliferation, migration, and invasion, while promoting apoptosis. In vivo, CLip@Sil significantly suppressed primary tumor growth and lung metastasis, extended overall survival, and exhibited minimal systemic toxicity. These findings highlight the value of combining competing endogenous RNA regulatory networks with nanomaterial based targeted delivery systems for GC therapy. The CLip@Sil platform offers a promising direction for the future development of precise and biomimetic nanotherapeutics in oncology.

胃癌（GC）仍然是一个主要的全球健康问题，需要更有效的治疗方法。在这项研究中，我们开发了一种新的仿生纳米囊泡系统-癌细胞膜包被脂质体纳米载体负载水飞蓟宾(CLip@Sil) -设计用于靶向治疗GC。通过整合网络药理学和转录组学分析，我们确定了13个关键靶基因，这些基因在PI3K/AKT和IL-17信号通路中显著富集，HSP90AA1是一个中心调控节点。进一步的机制研究发现水飞蓟宾通过调节SNHG1/miR-383-5p/HSP90AA1竞争内源性RNA （ceRNA）轴，从而抑制PI3K/AKT通路发挥其抗癌作用。该工程CLip@Sil系统通过其仿生癌症膜涂层证明了增强的肿瘤靶向能力，能够选择性地在肿瘤组织中传递和积累药物。体外研究证实CLip@Sil抑制GC细胞增殖、迁移和侵袭，同时促进细胞凋亡。在体内，CLip@Sil显著抑制原发肿瘤生长和肺转移，延长总生存期，并表现出最小的全身毒性。这些发现强调了将竞争性内源性RNA调控网络与基于纳米材料的靶向递送系统相结合用于GC治疗的价值。CLip@Sil平台为肿瘤精准和仿生纳米治疗的未来发展提供了一个有希望的方向。

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引用次数: 0

Strategies for overcoming multiple barriers of oral administration of protein and peptide therapeutics 克服蛋白质和肽治疗药物口服给药多重障碍的策略

IF 10.2 1区医学 Q1 ENGINEERING, BIOMEDICAL

Materials Today Bio

Pub Date : 2026-04-01 Epub Date: 2026-01-07 DOI: 10.1016/j.mtbio.2026.102763

Xiaofan Wang , Keke Wang , Yitan Fang , Youxi Zhang , Lixin Yi , Xiaohong Li , Qinfu Zhao , Xu Zhu , Shuang Cai , Long Wan

Oral delivery of protein and peptide therapeutics (PPs) offers a non-invasive, patient-friendly alternative to parenteral administration, yet faces multiple formidable barriers due to the complex gastrointestinal (GI) environment. This review provides an overview of the latest advances of strategies developed to overcome the four main GI barriers: the harsh pH environment, enzymatic degradation, the mucus layer, and the intestinal epithelial barrier. We critically evaluate various approaches including chemical modifications, permeation enhancers, encapsulation techniques, and novel delivery systems like microneedles and nanoparticle-based carriers, each designed to protect PPs and enhance their bioavailability. A comparative analysis of the advantages and limitations of these strategies is presented, along with a discussion on how to integrate them synergistically for the effective overcoming of multiple GI tract barriers. Furthermore, we examine the current challenges associated with oral PPs drug delivery systems and explore future directions aimed at achieving successful therapeutic outcomes.

口服蛋白质和肽疗法（PPs）提供了一种非侵入性的、对患者友好的肠外给药选择，但由于复杂的胃肠道（GI）环境，它面临着多重巨大的障碍。本文综述了克服四种主要胃肠道屏障的策略的最新进展：恶劣的pH环境、酶降解、黏液层和肠上皮屏障。我们批判性地评估了各种方法，包括化学修饰、渗透增强剂、封装技术和新型递送系统，如微针和纳米颗粒载体，每种方法都旨在保护PPs并提高其生物利用度。比较分析了这些策略的优点和局限性，并讨论了如何将它们协同整合以有效克服多种胃肠道障碍。此外，我们研究了目前与口服PPs药物递送系统相关的挑战，并探索了旨在实现成功治疗结果的未来方向。

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引用次数: 0

Injectable anti-inflammatory, antioxidant supramolecular nanofiber hydrogel for peripheral nerve injury repair and neuropathic pain relief 可注射抗炎、抗氧化的超分子纳米纤维水凝胶用于周围神经损伤修复和神经性疼痛缓解

IF 10.2 1区医学 Q1 ENGINEERING, BIOMEDICAL

Materials Today Bio

Pub Date : 2026-04-01 Epub Date: 2026-01-07 DOI: 10.1016/j.mtbio.2026.102780

Anqi Liu , Kui Sheng , Huihui Li , XinYang Zhao , Xiaojun Zhang , Haitao Su , Tsring Samdrup , Ye Zhang , Xianwen Hu , LiJun Weng , YaGuang Wang

Patients with peripheral nerve injury (PNI) often experience neuropathic pain (NP), which is difficult to treat effectively due to ongoing inflammation and oxidative stress that impede nerve repair. Traditional anti-inflammatory antioxidants are limited by short half-lives and significant side effects. This study introduces a supramolecular hydrogel formed by combining anti-inflammatory betamethasone phosphate (Betp) with calcium chloride to create betamethasone phosphate hydrogel (Betp@Gel). The antioxidant curcumin (Cur) was incorporated into this gel to form Cur/Betp@Gel, which can be injected directly at the injury site for sustained Cur release. Cur/Betp@Gel demonstrates superior sustained-release capabilities and therapeutic effectiveness compared to Betp@Gel or Cur alone. It enhances pain relief, supports functional recovery after nerve damage, and promotes nerve repair and regeneration. This is achieved by Betp@Gel's anti-inflammatory effects, which inhibit TNF-α, IL-1β, and IL-6, combined with Cur's continuous slow release, which scavenges reactive oxygen species (ROS). Additionally, Cur/Betp@Gel mitigates PNI-induced spinal inflammation by reducing GFAP and Iba-1 expression in the spinal cord. Overall, in-situ injection of Cur/Betp@Gel is a promising strategy for aiding nerve repair and alleviating neuropathic pain.

周围神经损伤（PNI）患者经常出现神经性疼痛（NP），由于持续的炎症和氧化应激阻碍神经修复，这种疼痛难以有效治疗。传统的抗炎抗氧化剂受半衰期短和显著副作用的限制。本研究介绍了一种将抗炎的磷酸倍他米松（Betp）与氯化钙结合形成的超分子水凝胶（Betp@Gel）。抗氧化剂姜黄素（Cur）加入到凝胶中形成Cur/Betp@Gel，可以直接注射到损伤部位，持续释放Cur。与Betp@Gel或单独使用Cur相比，Cur/Betp@Gel具有更好的缓释能力和治疗效果。它增强疼痛缓解，支持神经损伤后的功能恢复，促进神经修复和再生。这是通过Betp@Gel的抗炎作用，抑制TNF-α， IL-1β和IL-6，结合Cur的持续缓慢释放，清除活性氧（ROS）来实现的。此外，Cur/Betp@Gel通过降低脊髓中GFAP和Iba-1的表达来减轻pni诱导的脊髓炎症。总的来说，原位注射Cur/Betp@Gel是一种很有希望的帮助神经修复和减轻神经性疼痛的策略。

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引用次数: 0

Stiff matrix promotes lung cancer cell migration through down-regulating the Piezo1 channel expression to facilitate Ca2+-dependent filopodia formation 硬基质通过下调Piezo1通道表达促进Ca2+依赖性丝状足形成，从而促进肺癌细胞迁移

IF 10.2 1区医学 Q1 ENGINEERING, BIOMEDICAL

Materials Today Bio

Pub Date : 2026-04-01 Epub Date: 2026-01-12 DOI: 10.1016/j.mtbio.2026.102786

Xiaoling Jia , Lin Zhao , Juncheng Bai , Lu Wen , Qianyu Meng , Haikun Wang , Junqi Men , Hui Shao , Yingying Guo , Xinlan Chen , Xing Chen , Lin-Hua Jiang , Yubo Fan , Huawei Liu

Matrix stiffening profoundly influences cancer cell functions and cancer progression, and the mechanosensitive Piezo1 channel is implicated in these processes. Different from what is observed in most solid tumors, the Piezo1 channel in lung cancer is down-regulated and negatively regulates cancer cell migration, but the underlying mechanism is still unclear. Herein, we investigated the role of Piezo1 channel in matrix stiffness regulation of lung cancer cell migration and the mechanisms in A549 cells growing on polyacrylamide (PA) hydrogels with different stiffness. Compared with soft substrate, stiff substrate promoted cell migration, down-regulated Piezo1 expression, favored filopodia formation, as well as restraining the rise in intracellular calcium concentration ([Ca²⁺]_i). Additionally, blockade or knockdown of Piezo1 channel promoted, whereas its activation suppressed, cell migration and filopodia formation. Furthermore, reducing the [Ca²⁺]_i promoted cell migration and filopodia formation. Finally, stiff substrate induced cofilin phosphorylation, which was enhanced by inhibiting the Piezo1 channel or reducing the [Ca²⁺]_i and, conversely, suppressed by activating the Piezo1 channel. Collectively, our study has revealed that stiff matrix down-regulates the Piezo1 channel expression and thereby restrains the rise in the [Ca²⁺]_i to facilitate cofilin phosphorylation and filopodia formation, leading to an increase in lung cancer cell migration. These findings broaden our understanding of the molecular mechanism by which the Piezo1 channel functions in lung cancer differently from in other cancers.

基质硬化深刻影响癌细胞功能和癌症进展，而机械敏感的Piezo1通道参与了这些过程。与在大多数实体肿瘤中观察到的不同，肺癌中的Piezo1通道下调并负向调节癌细胞迁移，但其潜在机制尚不清楚。本文研究了Piezo1通道在基质刚度调节肺癌细胞迁移中的作用，以及在不同刚度的聚丙烯酰胺（PA）水凝胶上生长的A549细胞的机制。与软底物相比，硬底物促进细胞迁移，下调Piezo1表达，有利于丝状足的形成，抑制细胞内钙浓度（[Ca2+]i）的升高。此外，阻断或敲低Piezo1通道促进细胞迁移和丝状足形成，而其激活抑制细胞迁移和丝状足形成。此外，降低[Ca2+]i可促进细胞迁移和丝状足的形成。最后，刚性底物诱导cofilin磷酸化，通过抑制Piezo1通道或减少[Ca2+]i来增强，相反，通过激活Piezo1通道来抑制。总的来说，我们的研究表明，硬基质下调了Piezo1通道的表达，从而抑制了[Ca2+]i的升高，从而促进了cofilin的磷酸化和丝状足的形成，导致肺癌细胞迁移的增加。这些发现扩大了我们对Piezo1通道在肺癌中不同于其他癌症中的功能的分子机制的理解。

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引用次数: 0

Engineered prebiotic microcapsules Co-Encapsulating berberine and curcumin Elicit multi-synergistic therapy for ulcerative colitis 工程益生元微胶囊共封装小檗碱和姜黄素引发溃疡性结肠炎的多重协同治疗

IF 10.2 1区医学 Q1 ENGINEERING, BIOMEDICAL

Materials Today Bio

Pub Date : 2026-04-01 Epub Date: 2026-01-07 DOI: 10.1016/j.mtbio.2026.102778

Huanyu Li , Chuanyu Zhang , Ziwei Yang , Yifan Li , Dan Liu , Yanan Zhang , Lingmin Zhang , Ning Wang , Mingxin Zhang , Mingzhen Zhang , Zhaoxiang Yu , Xueyong Wei , Yujie Zhang

Background

Ulcerative colitis (UC) is a common type of inflammatory bowel disease, where the vicious cycle of inflammation and oxidative stress poses a major challenge in its treatment, and existing therapies have limitations. Berberine (BBR) and curcumin (CUR) have the potential for synergistic treatment of UC, but this potential has not been verified in UC. Additionally, both BBR and CUR suffer from poor water solubility and low bioavailability. This study aims to construct prebiotic microcapsules (BBR/CUR@MC) for the co-delivery of BBR and CUR and explore their therapeutic mechanism in UC.

Methods

Network pharmacology was used to predict the targets and pathways of BBR and CUR in UC. BBR/CUR@MC was prepared using microfluidic electrospray technology, and its colon targeting and biocompatibility were evaluated through in vivo experiments. In a Dextran sulfate sodium (DSS)-induced UC mouse model, the therapeutic effect was assessed using multiple indicators, and the mechanism of action was explored by transcriptome analysis.

Results

Network pharmacology showed that BBR and CUR can exert therapeutic effects on UC through synergistic regulation of TNF and AGE-RAGE signaling pathways. The successfully constructed BBR/CUR@MC had good colon targeting and biocompatibility. In the mouse colitis model, oral administration of BBR/CUR@MC inhibited ADAM17 in the TNF signaling pathway and MAPK11/13, COL4A1, and COL1A1 in the AGE-RAGE signaling pathway, thereby downregulating pro-inflammatory cytokines such as TNF-α and IL-1α, upregulating IL-10, scavenging ROS, significantly alleviating colonic inflammation and repairing the intestinal barrier in mice, with a therapeutic effect superior to that of single-drug microcapsules and 5-ASA.

Conclusion

BBR/CUR@MC can exert synergistic anti-inflammatory and antioxidant effects in UC treatment by regulating TNF and AGE-RAGE signaling pathways, providing a new multi-mechanism therapeutic strategy for UC.

背景溃疡性结肠炎（UC）是一种常见的炎症性肠病，炎症和氧化应激的恶性循环对其治疗构成了重大挑战，现有治疗方法存在局限性。小檗碱（BBR）和姜黄素（CUR）具有协同治疗UC的潜力，但这种潜力尚未在UC中得到证实。此外，BBR和CUR都存在水溶性差和生物利用度低的问题。本研究旨在构建益生元微胶囊（BBR/CUR@MC），用于BBR和CUR的共给药，并探讨其治疗UC的机制。方法应用网络药理学方法预测UC中BBR和CUR的作用靶点和通路。采用微流控电喷雾技术制备BBR/CUR@MC，通过体内实验对其结肠靶向性和生物相容性进行评价。在葡聚糖硫酸钠（DSS）诱导的UC小鼠模型中，采用多指标评价其治疗效果，并通过转录组分析探讨其作用机制。结果网络药理学研究表明，BBR和CUR可通过协同调节TNF和AGE-RAGE信号通路对UC发挥治疗作用。成功构建的BBR/CUR@MC具有良好的结肠靶向性和生物相容性。在小鼠结肠炎模型中，口服BBR/CUR@MC可抑制TNF信号通路中的ADAM17和AGE-RAGE信号通路中的MAPK11/13、COL4A1、COL1A1，从而下调小鼠的TNF-α、IL-1α等促炎细胞因子，上调IL-10，清除ROS，显著缓解结肠炎症，修复肠道屏障，治疗效果优于单药微胶囊和5-ASA。结论bbr /CUR@MC通过调节TNF和AGE-RAGE信号通路，在UC治疗中发挥协同抗炎和抗氧化作用，为UC提供了一种新的多机制治疗策略。

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引用次数: 0

NIR-II imaging-guided nanoplatform for synergistic mitochondria-targeted pyroptosis and macrophage reprogramming immunotherapy NIR-II成像引导纳米平台协同线粒体靶向焦亡和巨噬细胞重编程免疫治疗

IF 10.2 1区医学 Q1 ENGINEERING, BIOMEDICAL

Materials Today Bio

Pub Date : 2026-04-01 Epub Date: 2026-01-27 DOI: 10.1016/j.mtbio.2026.102860

Di Zhang , Xu He , Kannappan Vinodh , Zhehan Yao , Wanyu Wei , Jingxiang Liang , Ningbo Li , Zhifang Wu , Sijin Li

Cancer immunotherapy has revolutionized modern oncology by mobilizing the body’s immune system, yet its efficacy remains severely limited in immunologically “cold” tumors, which are defined by poor immune infiltration and low tumor immunogenicity. Here, we report a multi-functional nanoplatform that integrates a new second near-infrared (NIR-II) aggregation-induced emission luminogen (AIEgen), a mitochondria-targeted lonidamine prodrug, and cryo-shocked M1 macrophage membranes (CSMs) to achieve synergistic tumor microenvironment (TME) reprogramming and precision image-guided immunotherapy. The bright NIR-II AIEgen enables high-resolution fluorescence and photoacoustic imaging for real-time tumor visualization and photothermal therapy. The prodrug LND-1-PEG-24, cleavable by TME-overexpressed cathepsin B, preferentially accumulates in mitochondria to trigger caspase-3/GSDME-mediated pyroptosis, leading to the release of danger-associated molecular patterns that markedly enhance tumor immunogenicity. Simultaneously, CSMs promote durable polarization of tumor-associated macrophages (TAMs) toward the tumoricidal M1 phenotype via the TLR2/MAPK pathway, thereby alleviating TME immunosuppression. In tumor-bearing mice, this nanoplatform synergistically enhances cytotoxic T cell infiltration, reverses immune suppression, and effectively inhibits both primary tumor growth and metastatic progression through the activation of systemic antitumor immunity. This work establishes a versatile strategy that unifies NIR-II phototheranostics, mitochondria-targeting pyroptosis, and TAM reprogramming, providing a robust and targeted approach for cancer immunotherapy.

癌症免疫疗法通过调动人体的免疫系统，使现代肿瘤学发生了革命性的变化，但在免疫“冷”肿瘤中，其疗效仍然受到严重限制，这种肿瘤的免疫浸润性差，肿瘤免疫原性低。在这里，我们报道了一个多功能纳米平台，该平台集成了新的第二种近红外（NIR-II）聚集诱导发射发光原（AIEgen），线粒体靶向lonidamine前药和低温冲击M1巨噬细胞膜（cms），以实现协同肿瘤微环境（TME）重编程和精确图像引导免疫治疗。明亮的NIR-II AIEgen可实现高分辨率荧光和光声成像，用于实时肿瘤可视化和光热治疗。前药LND-1-PEG-24可被tme过表达的组织蛋白酶B切割，优先在线粒体中积累，触发caspase-3/ gsdme介导的焦亡，导致释放危险相关的分子模式，显著增强肿瘤的免疫原性。同时，csm通过TLR2/MAPK通路促进肿瘤相关巨噬细胞（tam）向肿瘤杀伤M1表型持久极化，从而减轻TME免疫抑制。在荷瘤小鼠中，该纳米平台协同增强细胞毒性T细胞浸润，逆转免疫抑制，并通过激活全身抗肿瘤免疫有效抑制原发肿瘤生长和转移进展。这项工作建立了一种统一NIR-II光治疗、线粒体靶向焦亡和TAM重编程的通用策略，为癌症免疫治疗提供了一种强大的靶向方法。

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引用次数: 0

Angiogenesis-facilitating and inflammation-modulating SIS-based patches coupled with functional peptides for abdominal wall repair 促进血管生成和炎症调节的基于sis的贴片与功能肽联合用于腹壁修复

IF 10.2 1区医学 Q1 ENGINEERING, BIOMEDICAL

Materials Today Bio

Pub Date : 2026-04-01 Epub Date: 2026-01-13 DOI: 10.1016/j.mtbio.2026.102795

Zhenyu Zou , Yuchen Liu , Xueying Zhang , Jinxin Cao , Pengfei Wei , Yiqian Huang , Wei Jing , Bo Zhao , Minggang Wang

Abdominal wall defects caused by trauma, tumors, infections, abdominal surgery, and congenital factors can lead to functional impairments. The use of patches remains the most effective treatment approach. However, current repair materials still have limitations in regulating inflammation and promoting vascularization. Here, a small intestinal submucosa (SIS) extracellular patch was developed via conjugation with functional peptides PR1P and LL37 (i.e., SIS-PR1P-LL37), to achieve angiogenesis and inflammation modulation for abdominal wall repair. In vitro experiments confirmed its superior pro-angiogenic potential when human umbilical vein endothelial cells (HUVECs) were treated with the patch, both tube formation (total tube length: 4.51 ± 0.53 mm, junction count: 28.00 ± 4.97) and scratch wound repair (repair area 3.26-fold that of the SIS group) outperformed the native SIS group (average tube length: ∼1.3 mm). After 7 days of culture, the VEGF expression was higher than that in the SIS group, and the expression levels of key angiogenic genes (VEGF, VEGFR-2, etc.) were 5.45–7.82-fold higher than those in the control group. Additionally, this peptide-conjugated SIS patch could enhance cell proliferation and angiogenic differentiation, effectively reduce the levels of inflammatory cytokines, and enrich the TLR and VEGF signaling pathways. The rat abdominal wall defect model further confirmed its superior capacity for tissue regeneration and angiogenesis, indicating it provides important theoretical and experimental support for the development of novel bioactive patches and holding promise for optimizing clinical strategies for abdominal wall repair.

创伤、肿瘤、感染、腹部手术和先天性因素引起的腹壁缺损可导致功能障碍。使用贴片仍然是最有效的治疗方法。然而，目前的修复材料在调节炎症和促进血管化方面仍有局限性。在这里，通过与功能肽PR1P和LL37（即SIS-PR1P-LL37）结合，开发了小肠粘膜下层（SIS）细胞外贴片，以实现血管生成和炎症调节，以修复腹壁。体外实验证实了该贴片对人脐静脉内皮细胞（HUVECs）具有优越的促血管生成潜力，管的形成（总管长：4.51±0.53 mm，结数：28.00±4.97）和划伤修复（修复面积是SIS组的3.26倍）均优于天然SIS组（平均管长：~ 1.3 mm）。培养7 d后，VEGF表达高于SIS组，关键血管生成基因（VEGF、VEGFR-2等）表达水平较对照组高5.45 - 7.82倍。此外，该肽偶联的SIS贴片可促进细胞增殖和血管生成分化，有效降低炎症细胞因子水平，丰富TLR和VEGF信号通路。大鼠腹壁缺损模型进一步证实了其优越的组织再生和血管生成能力，为开发新型生物活性贴片提供了重要的理论和实验支持，并有望优化腹壁修复的临床策略。

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引用次数: 0

Infection protection, immune regulation and epithelial regeneration trifunctional hydrogel for treatment of burn wounds 三功能水凝胶治疗烧伤创面的感染保护、免疫调节和上皮再生

IF 10.2 1区医学 Q1 ENGINEERING, BIOMEDICAL

Materials Today Bio

Pub Date : 2026-04-01 Epub Date: 2026-01-10 DOI: 10.1016/j.mtbio.2026.102788

Xingyue Chen , Jiachen Lu , Zhaojun Wu , Haopeng Zhang , Wei Zheng , Huanghe Zeng , Dongbiao Chang , Jie Weng , Jinsheng Li , Tailin Guo

Severe burn wounds are characterized by epithelial disruption and persistent inflammation, which impede re-epithelialization and heighten susceptibility to bacterial colonization and invasion, thereby posing serious clinical risks. To address these challenges, we developed an innovative smart hydrogel (Ag-IMP-U@Cur), in which uridine (U) is incorporated as a backbone-forming component via reversible boronate ester bonds with phenylboronic acid, thereby endowing the hydrogel with dual functions of acidic microenvironment responsiveness and promotion of re-epithelialization. The Ag-IMP complex serves as a structural scaffold that reinforces the network stability, while the combination of Ag-IMP and Cur-loaded ZIF-8 (Cur-ZIF-8) imparts controlled-release, antibacterial, and anti-inflammatory properties. In vitro and in vivo studies demonstrate that this hydrogel markedly suppresses infection and inflammation while accelerating wound closure. Collectively, this work introduces an innovative strategy that integrates a nucleoside unit, metal ions, and a phytochemical into a responsive multifunctional hydrogel, offering a promising therapeutic avenue for severe burn injuries.

严重烧伤创面的特点是上皮破坏和持续炎症，这阻碍了再上皮化，增加了细菌定植和入侵的易感性，从而带来了严重的临床风险。为了解决这些挑战，我们开发了一种创新的智能水凝胶（Ag-IMP-U@Cur），其中尿苷(U)通过与苯硼酸的可逆硼酸酯键结合作为骨架形成成分，从而赋予水凝胶双重功能，即酸性微环境响应性和促进再上皮化。Ag-IMP复合物作为结构支架，加强了网络的稳定性，而Ag-IMP和cu负载的ZIF-8 （cu -ZIF-8）的组合赋予了控释、抗菌和抗炎特性。体外和体内研究表明，这种水凝胶显著抑制感染和炎症，同时加速伤口愈合。总的来说，这项工作引入了一种创新的策略，将核苷单元、金属离子和植物化学物质整合到一种反应性多功能水凝胶中，为严重烧伤提供了一种有希望的治疗途径。

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引用次数: 0