JOURNAL OF CONTROLLED RELEASE控制释放杂志
JOURNAL OF CONTROLLED RELEASE(英文缩写 J CONTROL RELEASE),ISSN 0168-3659,eISSN 1873-4995,中文译名:控制释放杂志 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 | 11.467 | Q1 |
| 2022 | 10.800 | Q1 |
| 2023 | 10.500 | Q1 |
| 2024 | 11.500 | Q1 |
| 2025 | 12.400 | Q1 |
JOURNAL OF CONTROLLED RELEASE 最新收录文献
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1. Hybrid membrane-coated motors for atopic dermatitis therapy via pruritus relief and ILC2 suppression.
1. 用于特应性皮炎治疗的杂化膜涂层马达：通过缓解瘙痒和抑制ILC2发挥作用PMID:日期:2026-10-03Atopic dermatitis (AD) is a chronic, relapsing inflammatory skin disorder characterized by intense pruritus, xerosis, and erythema. Its pathogenesis involves hyperactivation of type 2 innate lymphoid cells (ILC2s) and excessive accumulation of interleukin-31. Moreover, over-colonization of Staphylococcus aureus exacerbates inflammation and skin barrier damage. Targeting pruritus and restoring immune and microbiota homeostasis are crucial for AD management. Herein, we developed a near-infrared-responsive anti-pruritic motor for AD treatment. The motor is encapsulated in a hybrid membrane armor composed of Cutibacterium acnes cell wall and keratinocytes membrane, enabling targeted ILC2 downregulation for immunomodulation and effective clearance of free interleukin-31 for pruritus relief. Inside the armor, a janus bowl-shaped polydopamine (Bowl-PDA) exhibits NIR-responsive motion under NIR irradiation, significantly enlarging the clearance area of the membrane armor. Concurrently, Zn released from the system effectively inhibits Staphylococcus aureus colonization. This integrated motor significantly reduced erythema and scratching-related indices, restored skin barrier and microbiota function, normalized ILC homeostasis by downregulating IL-33-ILC2 axis and suppressed IL-31-TRPV1 pruritic signaling. Collectively, this strategy demonstrates robust anti-pruritic efficacy, coordinated remodeling of immune and microbiota homeostasis, offering a promising platform for precision AD therapy.
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2. Delivery architectures for oligonucleotide therapeutics in genetic and rare diseases: GalNAc-based hepatocyte targeting and extrahepatic translation.
2. 遗传病和罕见病中寡核苷酸疗法的递送架构：基于GalNAc的肝细胞靶向及肝外转化PMID:日期:2026-10-03Many genetic and rare diseases are molecularly defined but remain difficult to treat because their biology involves intracellular targets, toxic gain-of-function mechanisms, splicing defects, repeat expansions, or chemically undruggable pathways. Although RNA medicines can be designed directly from genetic information, their clinical success depends on delivery architecture rather than sequence design alone. This review examines delivery architectures for oligonucleotide therapeutics, using GalNAc-siRNA as the central clinically validated model. The GalNAc-siRNA platform demonstrates how receptor selection, ligand presentation, linker design, chemical stabilization, intracellular persistence, PK/PD properties, dosing, and safety monitoring enable durable subcutaneous hepatocyte pharmacology. As of July 18, 2026, seven FDA-approved GalNAc-siRNA drugs validated this paradigm. We compare extrahepatic strategies for the CNS, muscle, eye, lung, kidney, immune cells, and adipose tissue. Intrathecal C16-siRNA and TfR1-directed antibody-oligonucleotide conjugates are among the most advanced extrahepatic approaches. Inhaled pulmonary RNAi has generated human PD and entered Phase 2a development; divalent CNS siRNA has entered Phase 1; adipose RNAi is in Phase 1/2a; ocular and kidney synthetic-siRNA platforms remain preclinical, whereas immune-cell delivery remains early translational. Antisense oligonucleotide and phosphorodiamidate morpholino oligomer examples illustrate shared delivery principles, including GalNAc-mediated hepatocyte targeting, TfR1-mediated muscle uptake, and local central nervous system and ocular administration. Rather than comprehensively reviewing oligonucleotide chemistry, this review emphasizes delivery architecture, including targeting moieties, lipophilic and structural handles, linker design, administration route, PK/PD, safety liabilities, rare-disease biomarkers, and regulatory experience. Overall, RNA medicines are genetically programmable, but their clinical reach is determined by delivery architecture.
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3. Structural DNA nanotechnology-guided spatially-ordered arrangement of aptamers on natural killer cells for solid tumor immunotherapy.
3. 结构DNA纳米技术引导的自然杀伤细胞上适体的空间有序排列用于实体瘤免疫治疗PMID:日期:2026-10-02While natural killer (NK) cells are able to kill malignant cells, NK-base immunotherapies of solid tumors remain limited due to lack of specific targeting. In this work, NK-92MI cells were artificially-engineered with two aptamers designed to specifically bind cancer cells. The strategy used a mild reduction strategy to install aptamer-associated Y-shaped backbone-rigidified three-dimensional DNA tetrahedrons (RDTs) on NK cells. The resulting d-RDT-NK cells exhibited a enhanced tumor-targeting ability in vitro. After systemic administration into a HeLa tumor-bearing BALB/c nude mouse model, the engineered cells accumulated in tumor tissues and exhibited enhanced tumor inhibition activity and lack of detectable systemic toxicity. This method offers insights into the potential application of backbone-mediated structural DNA nanotechnology in artificially engineering of immune effector cells for improved targeting, hopefully opening new avenues for the clinical applications of NK cell immunotherapy in solid tumors.
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4. Dual-glycolipid engineered vaccine platform empowers delivery route customization to intercept tumor lung metastasis.
4. 双糖脂工程化疫苗平台赋能递送途径定制化以拦截肿瘤肺转移PMID:日期:2026-10-02Pulmonary metastasis remains a lethal challenge, necessitating potent mRNA vaccines to establish proactive immune surveillance. Although lipid nanoparticles (LNPs) are the gold standard for delivery mRNA, the "PEG dilemma"-comprising immunogenicity and poor cellular engagement-critically limits their efficacy. Here, we developed a biocompatibility, PEG-free mRNA platform (SG-LNP) co-modified with sialic acid-dimyristoyl-glycerol (SA-DMG) and monosialotetrahexosylganglioside (GM1), enabling a customizable tissue-targeting delivery pathway. This platform leverages the SA-Siglec axis to target antigen-presenting cells (APCs), markedly enhancing APCs uptake and facilitating endosomal escape. Upon pulmonary inhalation, the vaccine directly targets pulmonary APCs, shortening immunological pathways and enabling in situ priming of multiple immune effector cells (dendritic cells, macrophages, natural killer cells, and T cells). Following intravenous administration, it selectively targets splenic APCs to orchestrate a systemic immune surveillance network. Furthermore, leveraging this vaccine platform with tunable delivery routes, we investigated the contributions of local and systemic immune toward the prevention of tumor lung metastasis. We found that inhaled SG-LNP elicit robust local immune activation, leading to markedly reduced melanoma infiltration in the lungs relative to conventional PEG-modified LNPs. Notably, systemic administration of SG-LNP drives more extensive expansion of circulating antigen-specific T cells and natural killer cells (NKs). This systemic mobilization effectively intercepts circulating tumor cells before pulmonary colonization, achieving complete prevention of pulmonary metastasis with 100% protective efficacy. Our findings demonstrate that systemic coordination outperforms localized activation in prophylactic of organ-specific metastasis, providing a strategic blueprint for the design and administration of next-generation PEG-free mRNA vaccines.
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5. A systemic-absorption-blocked (SEAL) nanoplatform for mRNA-based local immunotherapy.
5. 一种用于基于mRNA的局部免疫治疗的全身吸收阻断（SEAL）纳米平台PMID:日期:2026-10-02Rapid transport of locally delivered mRNA lipid nanoparticles (mRNA-LNPs) into systemic circulation induces off-target protein expression and undesired side effects. Here we describe a systemic-absorption-blocked (SEAL) nanoplatform that achieves efficient mRNA delivery to disseminated peritoneal tumors using LNPs with minimized systemic exposure. Intraperitoneal administration of SEAL LNPs significantly reduces unintended mRNA expression in the liver and spleen, while maintaining robust protein expression in peritoneal tumors. Incorporation of cationic helper lipid is demonstrated essential for SEAL LNPs to minimize their systemic exposure. Using an in vitro transwell model to simulate the mesothelial barrier, we further elucidate that SEAL LNPs favor clathrin-mediated endocytosis and Golgi apparatus less involved intracellular trafficking in mesothelial cells, leading to reduced capability to penetrate the mesothelium for lymphatic transport. Intraperitoneal delivery of IL-12 mRNA (mIL-12) using the SEAL platform generates localized IL-12 expression with reduced systemic toxicity, leading to potent antitumor effects in mice bearing colorectal cancer (CRC) peritoneal dissemination. Delivery of mRNA-encoded therapeutic proteins using this platform presents a promising strategy to address peritoneal carcinomatosis.
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6. Extracellular vesicles: rising stars among drug delivery systems?
PMID:日期:2026-10-02Engineered extracellular vesicles (EVs) are increasingly being lauded as the next generation of drug delivery systems. Their intrinsic biological properties as well as their ability to transport therapeutic drug molecules have generated enormous enthusiasm. In this opinion paper, the author recaps that many of the properties now presented as unique advantages of engineered EVs, including biocompatibility, low toxicity, cargo-loading capacity, and surface functionalization, have long been established features of synthetic lipid vesicles. However, the major obstacles that have limited clinical translation of multifunctional liposomes, particularly targeted liposomes, are also likely to pose substantial challenges for engineered targeted EVs. Rather than viewing engineered EVs as a revolutionary new class of nanocarriers, the author proposes that their development should be guided by the successes and limitations of liposome technology. Studying the lessons learned from liposome technology may help prevent repeating historical mistakes and facilitate the rational development of clinically translatable EV-based therapeutics.
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7. A lymph node-targeted nanoplatform reprograms metabolic and immune microenvironments via dual ACSL3/4 inhibition in lymphatic metastatic tumors.
7. 一种靶向淋巴结的纳米平台通过双重抑制ACSL3/4重塑淋巴转移肿瘤的代谢与免疫微环境PMID:日期:2026-10-01Lymph node metastasis in hepatocellular carcinoma depends heavily on lipid metabolic reprogramming, wherein the acyl-CoA synthetase long-chain family members ACSL3 and ACSL4 act as central survival hubs. However, single-target interventions often fail to curb metastasis due to the inherent metabolic plasticity and flexibility of tumors. Here, through retrospective clinical cohort analyses, we discovered that ACSL3 and ACSL4 are markedly co-upregulated in metastatic lymph nodes, driving malignant progression and poor prognosis. Driven by this finding, we engineered a lymph node-targeted nanoplatform (siACSL3/4@Gal-LNP) for the dual-gene inhibition, aiming to modulate lipid metabolism and validate its feasibility as a therapeutic target. Utilizing this platform, we elucidated an integrated metabolic axis comprising the ACSL3-mediated "metabolic shield" for ferroptosis resistance and the ACSL4-driven "metastatic spear" for enhanced invasion. Notably, we found that single-target inhibition of ACSL4 triggers a compensatory upregulation of ACSL3, which decreases the ferroptosis sensitivity of tumor cells. Leveraging this dual-inhibition capability, the siACSL3/4@Gal-LNP nanoplatform effectively overcomes adaptive escape, directly inducing a profound lipid collapse. This intervention reshapes membrane biophysics to suppress invasion and triggers ferroptosis. Concurrently, it depletes Tregs and downregulates PD-L1, effectively reprogramming the immunosuppressive microenvironment toward an immune-active state. Furthermore, we verified that siACSL3/4@Gal-LNP could greatly sensitize metastatic tumors to low-dose radiotherapy by blocking metabolic escape pathways, and markedly overcome tumor cell resistance to ferroptosis. Therefore, this "dismantling shield and breaking spear" strategy effectively disrupts the lipid metabolic plasticity and remodels the immune microenvironment, providing a highly potent and effective therapeutic strategy for lymph node metastatic tumors.
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8. Antitumor efficacy of PD-1 blocking antibody is enhanced through liposomal delivery and myeloid immune modulation.
8. 通过脂质体递送和髓系免疫调节增强PD-1阻断抗体的抗肿瘤疗效PMID:日期:2026-10-01Systemic monoclonal antibody therapy against the PD-1 immune checkpoint (anti-PD1) is efficacious in less than 40% of patients with solid tumors. Beyond T-cells, PD-1 is expressed on myeloid populations such as monocytes, dendritic cells, myeloid progenitors, and tumor-associated macrophages (TAMs) that also have a propensity to interact with nanoparticles. Here, we developed a liposomal anti-PD1 formulation (LAP) to exploit the interaction of lipid nanoparticles with macrophages, aiming to enhance antitumor efficacy. LAP demonstrated efficient antibody conjugation and target binding, a mean particle size of 89 nm, and intravenous administration was associated with rapid but transient elevation of circulating pro-inflammatory cytokines. While conventional anti-PD1 therapy resulted in a modest, but not statistically significant, inhibition of tumor growth compared to vehicle in the B16-F10 melanoma model, LAP significantly reduced tumor growth and improved survival, achieving complete tumor rejection in 67% of mice versus 17% with conventional antibody treatment. LAP remodeled the tumor immunologic milieu towards an immune permissive environment, with significant reduction of pro-tumoral of M2-TAMs, and increased ratio of cytotoxic-to-regulatory T-cell. Myeloid (CD11b) cell depletion diminished LAP antitumor efficacy without significantly altering pharmacokinetics, indicating a myeloid cell-dependent anticancer mechanism of action. Together with data showing that LAP did not increase systemic toxicities, these findings strongly support the clinical translation of LAP and liposomes as a platform delivery system that can be leveraged to enhance the efficacy of PD-1 blockade.
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9. Membrane disruption and biomolecular enrichment-enhanced antibacterial therapy using peroxisome-inspired virus-like nickel nanoparticles.
9. 类过氧化物酶体模拟病毒样镍纳米颗粒通过膜破坏和生物分子富集增强抗菌治疗PMID:日期:2026-09-30Efficient peroxidase mimetics-assisted therapeutic strategies have been developed to combat antibiotic-resistant pathogens with the overuse of antibiotics. Although promising, their antibacterial outcomes and clinical translation have been restricted by the bacterial targeting specificity, as well as the limited lifetime and diffusion distance of reactive oxygen species (ROS). Meanwhile, bacterial debris and their hazardous derivatives after antibacterial treatment can stimulate macrophages to produce pro-inflammatory factors and exacerbate inflammatory response. Herein, we develop a novel membrane disruption and biomolecular enrichment-enhanced antibacterial strategy with the assistance of smart peroxisome-inspired virus-like spiky nickel nanoparticles (SNNPs). The well-defined spiky surface of SNNPs endow them with the ability to capture bacteria and penetrate bacterial membranes, followed by the in situ catalytic generation of ROS to kill bacteria. Moreover, these SNNPs can efficiently remove bacterial debris after antibacterial treatment. Using an oral mucosal infection model, our well-developed system can kill bacteria and decrease the inflammatory response because of its Fenton-like catalytic activity, bacterial capture capability, and removal function of inflammatory-related mediators. Together, the design and presentation of our current system with synergistic functions of membrane disruption and biomolecular enrichment pioneer a promising biomimetic approach for oral infectious diseases, advancing the use of nano-sized catalysts in medicine.
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10. Corrigendum to "From discovery to therapeutic development of monoclonal antibodies" [J. Control. Release., Volume 396, 10 August 2026, Article 115034].
10. 对“从发现到治疗性开发单克隆抗体”的勘误[J. Control. Release., 第396卷, 2026年8月10日, 文章115034]PMID:日期:2026-09-29该文献暂无摘要。