Journal of Controlled Release最新文献

{"title":"Phosphatidylcholine-derived carriers facilitate brain tumor delivery and enhance glioblastoma therapy","authors":"Jiang Yu ,&nbsp;Zewei Tu ,&nbsp;Jiali Fan ,&nbsp;Kunjian Lei ,&nbsp;Zhouqi Meng ,&nbsp;Binfan Chen ,&nbsp;Zefeng Wang ,&nbsp;William Escobar ,&nbsp;Jiangbing Zhou","doi":"10.1016/j.jconrel.2025.113999","DOIUrl":"10.1016/j.jconrel.2025.113999","url":null,"abstract":"<div><div>Glioblastoma (GBM) is the most common primary brain cancer without effective treatment. The ineffective treatment of GBM can be partially attributed to the existence of the blood-brain barrier (BBB). Lipids, which constitute over half the weight of the brain and play a vital role in brain tumor biology, can be transported to the brain in the form of lysophosphatidylcholines (LPCs) via specific LPC transporters at the BBB. We hypothesize that LPC analogs could be used as carriers for drug delivery to tumors in the brain. To test this hypothesis, we synthesized and screened a collection of LPC analogs, among which LPC analog 3 (A3), featuring a glycerophosphorylcholine (GPC) headgroup and a 15‑carbon tail, exhibited a marked ability to penetrate brain tumors. We characterized A3 as a carrier for drug delivery to brain tumors by using Doxorubicin (Dox) as the therapeutic payload and found that the A3-Dox conjugate with a cathepsin B-cleavable linker has a great ability to accumulate in brain tumors, leading to effective treatment of GBM without inducing significant cytotoxicity. Our study suggests a novel approach to improving the treatment of GBM by enhancing the delivery of therapeutic agents to the brain using A3 as a carrier.</div></div>","PeriodicalId":15450,"journal":{"name":"Journal of Controlled Release","volume":"385 ","pages":"Article 113999"},"PeriodicalIF":10.5,"publicationDate":"2025-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144566563","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A super-long-acting anti-PD-L1 nanobody fused to elastin-like polypeptide for triple-negative breast cancer immunotherapy","authors":"Qiongqiong Yao ,&nbsp;Fan Zhang ,&nbsp;Zhaoying Yang ,&nbsp;Yuanzi Sun ,&nbsp;Weiping Gao","doi":"10.1016/j.jconrel.2025.114002","DOIUrl":"10.1016/j.jconrel.2025.114002","url":null,"abstract":"<div><div>The limited tumor penetration of monoclonal antibodies or the rapid renal clearance of nanobodies hamper their application in cancer immunotherapy. Through genetic engineering, we fuse a thermosensitive elastin-like polypeptide of ELP(V) with a nanobody of KN035 that binds specifically to human programmed cell death protein ligand 1 (PD-L1) to generate a conjugate of KN035-ELP(V) for triple-negative breast cancer (TNBC) therapy. The high affinity of KN035-ELP(V) enables it to efficiently block the interaction of PD1 and PD-L1. A single intraperitoneal administration of KN035-ELP(V) leads to the <em>in situ</em> generation of a sustained-release depot, showing a circulating half-life that is 276.4-fold and 5.1-fold longer than those of KN035 and KN035 fused with fragment crystallizable (KN035-Fc), respectively. Additionally, KN035-ELP(V) outperforms KN035 and KN035-Fc in term of accumulation and penetration in tumor tissue. Compared to KN035 and KN035-Fc treatments, a single injection of KN035-ELP(V) induces a durable and efficient antitumor immunity in TNBC-bearing mice, resulting in improved anti-tumor efficacy with reduced adverse effects. Therefore, KN035-ELP(V) is promising as a super-long-acting anti-PD-L1 nanobody for efficient cancer immune checkpoint blockade therapy.</div></div>","PeriodicalId":15450,"journal":{"name":"Journal of Controlled Release","volume":"385 ","pages":"Article 114002"},"PeriodicalIF":10.5,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144533819","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hematite-embedded mesoporous nanoparticles for ferroptosis-inducing cancer sonoimmunotherapy","authors":"Jeongjin Lee ,&nbsp;Seung Woo Choi ,&nbsp;Minsung Park ,&nbsp;Wooram Um ,&nbsp;Seunglee Kwon ,&nbsp;Chan Ho Kim ,&nbsp;Hyeyeon Joo ,&nbsp;Dong Gil You ,&nbsp;Jae Ah Lee ,&nbsp;Sol Shin ,&nbsp;Heegun Kang ,&nbsp;Farrokhroo Ghahari ,&nbsp;Jaeyun Kim ,&nbsp;Jae Hyung Park","doi":"10.1016/j.jconrel.2025.113990","DOIUrl":"10.1016/j.jconrel.2025.113990","url":null,"abstract":"<div><div>Sonodynamic therapy (SDT) aims to treat cancers by generating reactive oxygen species in response to ultrasound (US). However, the clinical applications of SDT are often constrained due to its limited efficacy in triggering systemic immune responses. Considering this, we developed hematite-embedded PEGylated mesoporous silica nanoparticles (H@PMSNs) as potential sonosensitizers for inducing immunogenic cancer cell death. When B16F10 cells were exposed to H@PMSNs under US irradiation, the intracellular levels of glutathione and glutathione peroxidase 4 were significantly reduced, leading to lipid peroxidation of the cell membrane and triggering ferroptosis. Notably, after their systemic administration into tumor-bearing mice, H@PMSNs effectively inhibited tumor growth under US irradiation by inducing ferroptosis. This process led to the enhanced maturation of dendritic cells and a significant increase in cytotoxic T cells. Consequently, the antitumor efficacy of immune checkpoint blockade was significantly enhanced by H@PMSN-based SDT. The results of this study indicate that H@PMSNs, which induce the immunogenic death of cancer cells through hematite-mediated ferroptosis, could be promising sonosensitizers for cancer immunotherapy.</div></div>","PeriodicalId":15450,"journal":{"name":"Journal of Controlled Release","volume":"385 ","pages":"Article 113990"},"PeriodicalIF":10.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144521213","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"In memoriam: Professor Rimona Margalit (1941–2024)","authors":"Yaron Dekel ,&nbsp;Smadar Cohen ,&nbsp;Dan Peer","doi":"10.1016/j.jconrel.2025.113994","DOIUrl":"10.1016/j.jconrel.2025.113994","url":null,"abstract":"","PeriodicalId":15450,"journal":{"name":"Journal of Controlled Release","volume":"385 ","pages":"Article 113994"},"PeriodicalIF":10.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144524233","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cancer-associated fibroblast-derived extracellular vesicles loaded with GLUT1 inhibitor synergize anti-PD-L1 to suppress tumor growth via degrading matrix stiffness and remodeling tumor microenvironment","authors":"Yali Wu ,&nbsp;Wenjuan Chen ,&nbsp;Jingjing Deng ,&nbsp;Xingyu Zhou ,&nbsp;Jiangbin Chen ,&nbsp;Zimo Yang ,&nbsp;Xinghui Cao ,&nbsp;Jiatong Liu ,&nbsp;Qi Tan ,&nbsp;E. Zhou ,&nbsp;Minglei Li ,&nbsp;Mengfei Guo ,&nbsp;Yang Jin","doi":"10.1016/j.jconrel.2025.113998","DOIUrl":"10.1016/j.jconrel.2025.113998","url":null,"abstract":"<div><div>Cancer immunotherapy has transformed cancer treatment, demonstrating the potential for lasting responses in multiple solid and hematologic malignancies and thus has revolutionized cancer treatment in clinic. However, the intricate tumor microenvironment (TME), characterized by a rigid extracellular matrix (ECM) and robust immunosuppressive environment, presents substantial hurdles to the effectiveness of cancer immunotherapy. Thus, cancer-associated fibroblasts (CAFs), the most abundant stromal cells that mediate ECM remodeling and participate in immune suppression, represent promising therapeutic targets for combination immunotherapy. In this study, by using and analyzing single-cell RNA-sequencing (scRNA-seq) in the public datasets, we have identified the elevated expression of glucose transporter 1 (GLUT1) in activated CAF subgroups within tumor sites compared to normal tissues. Moreover, the recent literature has also demonstrated that CAFs undergoing high metabolic levels have been identified to show a better response to immunotherapy. Furthermore, extracellular vesicles (EVs) secreted by CAFs remain unexplored, and their role in drug transport systems and targeting efficiency towards tumorous cells remains uninvestigated. Herein, we identified the elevated expression of glucose transporter 1 (GLUT1) as a prognostic indicator for cancer associated with poor prognosis and investigated the vulnerability of lung tumor cell lines and CAFs to pharmacological GLUT1 inhibition with BAY-876. Based on the possibility of targeting the intrinsic TME-associated metabolism by GLUT1 inhibition, we have firstly employed CAFs-derived extracellular vesicles (cEVs) as a carrier for targeted delivery of BAY-876 into GLUT1-high CAFs and tumor cells. The cEV-BAY-876 (cEV<img>B6) treatment significantly resulted in glucose-rich, low-lactate TME, reversed the activated CAFs phenotype, enabled stromal reprogramming, decreased ECM stiffness and enhanced the infiltration of CD3 + CD8+ T cells in tumor core, thereby achieving an excellent anti-tumor efficiency. Moreover, cEV-B6 treatment synergized anti-programmed death ligand 1 (antiPD-L1) to reinvigorate the exhausted lymphocytes and exerted strong anticancer effects against mice lung tumors. Our study provides the first evidence that tumor stroma-specific therapies by targeting glucose metabolism present a promising strategy of remodeling the extracellular matrix to reverse CAFs into normal type and potentiate cytotoxic T lymphocytes (CTLs) infiltration thereby improving anticancer immunotherapy.</div></div>","PeriodicalId":15450,"journal":{"name":"Journal of Controlled Release","volume":"385 ","pages":"Article 113998"},"PeriodicalIF":10.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144521331","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A multivalent 9-O-acetylated sialic acid-conjugated bacteriophage platform for antiviral and immunomodulatory therapy for human coronavirus OC43","authors":"Palaniyandi Muthukutty ,&nbsp;Jinhyo Chung ,&nbsp;Sehoon Kim ,&nbsp;Hwa Young Kim ,&nbsp;Sang Hyun Lee ,&nbsp;Yewon Kim ,&nbsp;Woo-Jae Chung ,&nbsp;So Young Yoo","doi":"10.1016/j.jconrel.2025.113996","DOIUrl":"10.1016/j.jconrel.2025.113996","url":null,"abstract":"<div><div>Coronaviruses pose significant global health and economic challenges due to their capacity for rapid mutation and immune evasion, which limit the effectiveness of current treatments. Here, we present an engineered antiviral platform based on filamentous bacteriophages conjugated with multivalent 9-<em>O</em>-acetylated sialic acid ligands (Ac-SLPhage), designed to target conserved viral entry pathways of human coronavirus OC43 (HCoV-OC43), a surrogate for SARS-CoV-2. This nanomaterial competitively blocks viral attachment through high-affinity interactions with host sialic acid receptors, while simultaneously modulating host responses by enhancing antioxidant defenses and suppressing inflammation. Comprehensive structural and biophysical analyses confirmed efficient ligand presentation and viral binding. In vitro assays demonstrated robust inhibition of OC43 infectivity, restoration of cell viability, and suppression of pro-inflammatory cytokines. In vivo studies using a murine model validated the therapeutic efficacy of Ac-SLPhage, with improved survival, reduced viral loads, lung-targeted biodistribution, anti-inflammatory macrophage polarization and minimal immunogenicity. These results position Ac-SLPhage as a dual-function nanomaterial for antiviral and immunomodulatory therapy, offering broad applicability for respiratory coronavirus infections, including SARS-CoV-2, and contributing to pandemic preparedness strategies.</div></div>","PeriodicalId":15450,"journal":{"name":"Journal of Controlled Release","volume":"385 ","pages":"Article 113996"},"PeriodicalIF":10.5,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144516200","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Liposomal all-trans retinoic acid boosts anti-tumor immunity of radiotherapy via mitigating cancer stemness and remedying tumor microenvironment","authors":"Huilan He ,&nbsp;Yun Zheng ,&nbsp;Jinlong Ji ,&nbsp;Chunlian Ye ,&nbsp;Yu Sun ,&nbsp;Yuwei Peng ,&nbsp;Ying Zhang ,&nbsp;Zhiyuan Zhong","doi":"10.1016/j.jconrel.2025.113995","DOIUrl":"10.1016/j.jconrel.2025.113995","url":null,"abstract":"<div><div>Radiotherapy (RT) induces immunogenic cell death but also promotes immunosuppression, cancer stemness and immune evasion, thus compromising anti-tumor immune response and leading to cancer recurrence and metastasis. Here, we developed liposomal all-trans retinoic acid nanoparticles (LATRA) to simultaneously mitigate cancer stemness and remedy suppressive tumor microenvironment, which on one hand decreases tumorigenicity and sensitizes tumors to RT and on the other hand stimulates dendritic cell maturation and reprograms macrophages toward a pro-inflammatory M1 phenotype. In murine colorectal tumor model, RT combined with LATRA essentially reduces tumor burden, prevents recurrence and induces a durable immune response with memory effects. Notably, LATRA effectively eradicates residual tumor cells in post-surgery 4T1 breast tumor model, avoiding tumor relapse and lung metastasis. Liposomal all-trans retinoic acid offers a new and promising strategy to empower RT-induced anti-tumor immunity.</div></div>","PeriodicalId":15450,"journal":{"name":"Journal of Controlled Release","volume":"385 ","pages":"Article 113995"},"PeriodicalIF":10.5,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144521332","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"In situ antigen-capture strategies for enhancing dendritic cell-mediated anti-tumor immunity","authors":"Jingben Zheng ,&nbsp;Xiaoye Li ,&nbsp;Ao He ,&nbsp;Yu Zhang ,&nbsp;Yuebo Yang ,&nbsp;Meng Dang ,&nbsp;Qiang Li ,&nbsp;Yongbin Mou ,&nbsp;Heng Dong","doi":"10.1016/j.jconrel.2025.113984","DOIUrl":"10.1016/j.jconrel.2025.113984","url":null,"abstract":"<div><div>Dendritic cell (DC)-mediated tumor immunotherapy has demonstrated considerable potential, effectively bridging tumor antigens with specific anti-tumor immune responses. However, the heterogeneous and immunosuppressive tumor microenvironment (TME) frequently impairs DC function by inhibiting antigen uptake, restricting differentiation into mature DCs (mDCs), and limiting migration to tumor-draining lymph nodes (TDLNs), ultimately resulting in immune tolerance that diminishes specific anti-tumor immune responses. To overcome these limitations and effectively restore the DC-mediated link between tumor-derived antigens and robust anti-tumor immunity, nanovaccines utilizing in situ antigen-capture strategies have been developed. These strategies uniquely offer personalized and targeted activation of anti-tumor immune responses. In this review, we first address the influence of the TME on DC functionality, highlighting the numerous immunosuppressive factors that restrict efficient antigen uptake by DCs. Subsequently, we detail the core mechanisms underlying in situ antigen-capturing nanovaccines (AC-NVs), including covalent, noncovalent, and combined antigen capture methods. Furthermore, recent advances in AC-NVs constructed from various biomaterials are reviewed, emphasizing their intrinsic material properties and antigen-capturing capabilities for functionalizing DCs and enhancing specific anti-tumor immunity. Finally, we discuss current challenges and future perspectives for AC-NVs, emphasizing their potential role in developing personalized cancer vaccines, optimizing immune responses, and facilitating clinical translation.</div></div>","PeriodicalId":15450,"journal":{"name":"Journal of Controlled Release","volume":"385 ","pages":"Article 113984"},"PeriodicalIF":10.5,"publicationDate":"2025-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144515553","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Biocompatible self-illuminating sphingomyelin nanosystems for photodynamic-based cancer therapy","authors":"M. Abal-Sanisidro ,&nbsp;A. Palencia-Campos ,&nbsp;L. Ruiz-Cañas ,&nbsp;J. García-Fernández ,&nbsp;L. Cañada-García ,&nbsp;S. Batres-Ramos ,&nbsp;R. López-López ,&nbsp;R. Moreno ,&nbsp;M. Martín-Pastor ,&nbsp;B. Sainz Jr ,&nbsp;M. de la Fuente","doi":"10.1016/j.jconrel.2025.113982","DOIUrl":"10.1016/j.jconrel.2025.113982","url":null,"abstract":"<div><div>In recent years, personalized medicine has emerged as a key approach to potentially treat numerous diseases, in particular cancer. Within this field, nanotechnology has arisen as a promising tool with multiple biomedical applications, and organic nanoparticles stand out due to their improved translational prospects, primarily attributed to their biocompatibility and biodegradability. In this context, sphingomyelin nanoemulsions (SNs) are promising carriers for the delivery of innovative therapeutics and the advancement of novel anticancer therapeutics. Herein, we aimed to develop a new and novel type of biocompatible and biodegradable self-illuminating (SI) nanosystems for the treatment of pancreatic cancer by photodynamic therapy (PDT), upon association of the bioluminescent protein RLuc8 to SNs, and encapsulation of the photosensitizer Rose Bengal (SI-SNs). We present here a deep characterization of the developed SI-SNs and a first <em>in vitro</em> and <em>in vivo</em> proof of concept, highlighting the potential of this strategy for the development of innovative nanotherapeutics for pancreatic cancer.</div></div>","PeriodicalId":15450,"journal":{"name":"Journal of Controlled Release","volume":"385 ","pages":"Article 113982"},"PeriodicalIF":10.5,"publicationDate":"2025-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144515149","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ultrasound-activated nanovesicles for adenosine exhaustion and immune checkpoint blockade in cancer immunotherapy","authors":"Zesheng Li ,&nbsp;Beibei Zhang ,&nbsp;Shaobo Duan ,&nbsp;Ruiqing Liu ,&nbsp;Yuzhou Wang ,&nbsp;Yongchao Wang ,&nbsp;Juan Zhang ,&nbsp;Rong Huang ,&nbsp;Ru Jiang ,&nbsp;Rui Zhang ,&nbsp;Qi Zhou ,&nbsp;Linlin Zhang ,&nbsp;Xiaoxia Xu ,&nbsp;Yingying Zhao ,&nbsp;Si Chen ,&nbsp;Yue Yuan ,&nbsp;Xiaoxiao Li ,&nbsp;Lianfeng Mo ,&nbsp;Xu Zhang ,&nbsp;Siyi Yang ,&nbsp;Lianzhong Zhang","doi":"10.1016/j.jconrel.2025.113988","DOIUrl":"10.1016/j.jconrel.2025.113988","url":null,"abstract":"<div><div>Conventional antitumor therapies induce immunogenic cell death (ICD), releasing large amounts of ATP that are rapidly converted into immunosuppressive adenosine within the tumor microenvironment (TME). This accumulation of adenosine promotes tumor immune evasion by inhibiting effector immune cells and upregulating inhibitory immune checkpoints. To overcome this challenge, we designed ultrasound (US)-activated nanovesicle system ADA/Ce6@tLipo which is composed of T cell membranes displaying multiple immune checkpoint molecules and a liposome encapsulating chlorin e6 (Ce6) and adenosine deaminase (ADA). Upon US exposure, these nanovesicles generate reactive oxygen species (ROS) to induce ICD and initiate an antitumor immune response. Concurrently, ADA converts adenosine, produced from ATP breakdown following ICD, into inosine, reversing adenosine-mediated immunosuppression and enhancing T cell activation. Furthermore, the immune checkpoint molecules displayed on the nanovesicles block immune checkpoint ligands on tumor cells, boosting T cell activity and preventing exhaustion. ADA/Ce6@tLipo reprograms the TME by modulating adenosine metabolism and inhibiting multiple immune checkpoints, thereby amplifying T cell-mediated antitumor immunity. This approach offers a promising strategy to enhance the efficacy of cancer immunotherapy.</div></div>","PeriodicalId":15450,"journal":{"name":"Journal of Controlled Release","volume":"385 ","pages":"Article 113988"},"PeriodicalIF":10.5,"publicationDate":"2025-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144515153","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}