JOURNAL OF BIOMEDICAL SCIENCE生物医学科学杂志
JOURNAL OF BIOMEDICAL SCIENCE(英文缩写 J BIOMED SCI),ISSN 1021-7770,eISSN 1423-0127,中文译名:生物医学科学杂志 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 | 12.771 | Q1 |
| 2022 | 11.000 | Q1 |
| 2023 | 9.000 | Q1 |
| 2024 | 12.100 | Q1 |
| 2025 | 14.500 | Q1 |
JOURNAL OF BIOMEDICAL SCIENCE 最新收录文献
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1. Endothelial ADAM17 facilitates neutrophil migration and pulmonary microvascular permeability in acute lung inflammation.
1. 内皮细胞ADAM17在急性肺部炎症中促进中性粒细胞迁移和肺微血管通透性PMID:日期:2026-09-28Acute respiratory distress syndrome (ARDS) is characterized by endothelial barrier disruption, excessive neutrophil recruitment, and sustained pulmonary inflammation. The A Disintegrin and Metalloproteinase 17 (ADAM17) regulates inflammatory signaling through ectodomain shedding of adhesion molecules and cytokine receptors, yet its endothelial-specific contribution to acute lung injury remains poorly defined. Endothelial ADAM17 was deleted in ADAM17 Tie2-Cre mice using the Cre/loxP system. Acute lung inflammation was induced by lipopolysaccharide (LPS) inhalation. Systemic ADAM17 blockade was achieved by intraperitoneal TAPI‑1 or ADAM17/ADAM10 inhibition by GW280264X, administered 1 h before LPS. Pulmonary microvascular permeability was quantified by Evans Blue extravasation. Neutrophil trafficking across lung compartments (intravascular, endothelial adherent, interstitial, intra‑alveolar) was assessed by flow cytometry. Endothelial ADAM17 emerged as a central regulator of vascular permeability, neutrophil trafficking, and inflammatory amplification in LPS-induced acute pulmonary inflammation. LPS markedly increased pulmonary ADAM17 expression, whereas endothelial-specific deletion reduced total lung ADAM17 mRNA by 77.5%, highlighting the dominant endothelial contribution. Endothelial ADAM17 deficiency preserved endothelial junction integrity through maintenance of JAM-A surface expression and was associated with preserved expression of VE-cadherin and the tight junction proteins ZO-1, occludin, and claudin-5, thereby reducing protein-rich pulmonary edema. These changes were accompanied by enhanced neutrophil transmigration into interstitial and alveolar compartments through altered PSGL-1 and CD49d expression. Mechanistically, endothelial ADAM17 enhanced TNF receptor 1 and IL-6 receptor signaling, elevating TNF-α, myeloperoxidase, and neutrophil elastase levels. Pharmacological ADAM17 inhibition recapitulated the protective phenotype of endothelial ADAM17 deficiency, attenuating neutrophil recruitment, preserving endothelial barrier integrity, and limiting vascular leakage. These findings strengthen the evidence that endothelial ADAM17 is a key driver of inflammatory vascular dysfunction in ARDS and support ADAM17 as a rational therapeutic target.
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2. miR-196a reduces mutant Huntingtin aggregates by Rad23b-mediated degradation in Huntington's disease.
2. miR-196a通过Rad23b介导的降解减少亨廷顿病中的突变型亨廷顿蛋白聚集体PMID:日期:2026-09-24Huntington's disease (HD) is a neurodegenerative disorder caused by abnormal expansions of poly-glutamine repeats in the mutant Huntingtin (mHTT). The expanded proteins form pathological aggregates to disrupt neuronal functions during disease progression, suggesting the clearance of the aggregates is considered as a potential direction for development of therapy. Our previous studies have demonstrated one specific microRNA, miR-196a, downregulates mHTT aggregates and improves the pathological phenotypes in HD. However, the detailed mechanism remains unclear. Proteomic analyses and bioinformatic tools were used to identify putative miR-196a targets in HD, and the expression of one target gene, Rad23b, was manipulated in different HD models to assess its role in mHTT aggregates. Here, we identify Rad23b as a key target, and miR-196a directly downregulates Rad23b to reduce mHTT aggregates and toxicity. We also show Rad23b overexpression worsens mHTT pathology, while its knockdown or knockout diminishes aggregates, primarily through the ubiquitin-proteasome system (UPS). Moreover, Rad23b interacts with mHTT aggregates via its ubiquitin-binding domains, and promotes their ubiquitination; however, Rad23b disrupts the chymotrypsin-like activity of UPS, and contributes to mHTT accumulation. In transgenic mouse models in vivo, Rad23b increases mHTT aggregates and cell death in brains, and also worsens motor dysfunction in HD transgenic mice. These findings demonstrate that critical role of Rad23b in miR-196a-reduced pathological aggregates, and highly suggest downregulating Rad23b or disrupting its interaction with mHTT may offer novel strategies to mitigate mHTT aggregates to delay disease progression.
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3. The role of classical protein tyrosine phosphatases in diabetic kidney disease and therapeutic implications.
3. 经典蛋白酪氨酸磷酸酶在糖尿病肾病中的作用及治疗意义PMID:日期:2026-09-02Approximately one-third of people with diabetes have diabetic kidney disease (DKD), and DKD remains a leading cause of kidney failure in the United States. DKD is characterized by injury to the glomerular filtration barrier and renal tubulointerstitium, arising from complex and convergent metabolic, hemodynamic, and inflammatory insults. Tyrosine phosphorylation, a reversible post-translational modification, is a central regulatory mechanism in these pathways and is dynamically controlled by protein tyrosine kinases (PTKs) and protein tyrosine phosphatases (PTPs). Aberrant tyrosine phosphorylation is a hallmark of DKD and implicates PTPs as key modulators of podocyte, endothelial, tubular, and immune cell dysfunction. Over 100 genes code for PTPs in humans, with 38 'classical' PTPs that specifically target tyrosine motifs, including receptor-type and non-receptor-type subtypes. Several classical PTPs are implicated in DKD pathogenesis, while others are increasingly associated with signaling cascades that drive renal metabolism, inflammation, fibrosis, and cell death. There is growing interest in PTPs as their contributions to the disease emerge, though the role(s) of some remain uncharacterized in DKD. Moreover, recent breakthroughs in pharmaceuticals targeting PTPs for metabolic diseases and cancer have ignited interest in repurposing or tailoring PTP‑directed therapeutics for DKD. This review summarizes current knowledge and recent advances of classical PTPs in DKD, including their roles in insulin signaling, cellular architecture, and glomerular and tubular cell injury. It further discusses existing DKD treatments and highlights emerging strategies to pharmacologically modulate PTP activity, such as active‑site inhibitors, allosteric agents, and antibody‑targeting approaches. By integrating mechanistic insights with drug discovery efforts, this review outlines how targeting specific PTPs could complement current standard‑of‑care therapies and open new avenues for precision treatment of DKD.
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4. Artificial intelligence for translational personalized neoantigen cancer vaccine development.
4. 人工智能用于转化型个体化新抗原癌症疫苗开发PMID:日期:2026-08-31Personalized neoantigen cancer vaccine is a promising strategy for precision immunotherapy by targeting patient-specific and mutation-derived tumor antigens. Early clinical studies have demonstrated the feasibility, safety, and immunogenicity of these vaccines across multiple solid tumors, with encouraging outcomes particularly when combined with immune checkpoint blockade. However, broader clinical translation remains limited by sequential bottlenecks across the vaccine development pipeline, including false-positive neoantigen selection, imperfect modeling of antigen processing and HLA presentation, limited prediction of T-cell receptor recognition, and challenges in formulation, delivery, and manufacturing. Artificial intelligence and advanced computational workflows are increasingly integrated into this pipeline to improve candidate prioritization and support more reproducible decision-making. In this review, we summarize clinical progress and key translational barriers in personalized neoantigen vaccination, and discuss how AI-enabled approaches may contribute across four major stages: multi-omics integration for neoantigen discovery, processing-aware HLA presentation prediction, structure-aware and TCR-informed immunogenicity modeling, and data-driven formulation optimization, particularly for lipid nanoparticle-based delivery systems. These approaches are able to help narrow biological and chemical search spaces, improve prioritization, and provide mechanistic insights into antigen presentation and immune recognition rather than replacing experimental validation. This articlefurther addresses future implementation challenges, including dataset diversity, model interpretability, prospective benchmarking, manufacturing traceability, and evolving regulatory frameworks for individualized mRNA cancer immunotherapies. Integrating computational innovation with rigorous immunological validation, scalable manufacturing, and regulatory oversight will be essential for advancing personalized neoantigen vaccines toward broader clinical implementation.
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5. Glucose-dependent insulinotropic polypeptide receptor agonism improves heart failure with antifibrosis through Akt-dependent nitric oxide signaling.
PMID:日期:2026-08-31Cardiac fibrosis is a pathological remodeling process that contributes to the development and progression of heart failure. Although glucose-dependent insulinotropic polypeptide (GIP) may exert antifibrotic effects, how GIP receptor activation regulates cardiac fibrogenesis and modulates cardiac function in heart failure remains unclear. This study investigated whether GIP receptor agonism suppresses cardiac fibroblast activity and improves heart failure and explored the underlying mechanisms by using cellular and animal models. Human cardiac fibroblasts were treated with [D-Ala]GIP (DA-GIP; 10, 100, or 300 nM) for 24 h or left untreated (control). Fibroblast migration, collagen production, and intracellular signaling were examined using wound healing, immunoblotting, enzyme-linked immunosorbent, and fluorometric assays. Cardiac structure, function, and fibrosis were assessed through echocardiography and Masson's trichrome staining in rats with isoproterenol-induced heart failure with and without DA-GIP (24 nM/kg, twice daily for 2 weeks) administration. Compared with control cells, DA-GIP (300 nM)-treated cardiac fibroblasts exhibited a significantly lower migratory activity and reduced expression levels of pro-collagen IA1, pro-collagen III, and transforming growth factor-β1 proteins. Additionally, DA-GIP increased nitric oxide (NO) production and promoted endothelial NO synthase (eNOS) and protein kinase B (Akt) activation in cardiac fibroblasts. Notably, Akt inhibition blocked DA-GIP-induced eNOS activation, and treatment with N-nitro-L-arginine methyl ester (a NO synthase inhibitor, 100 μM) attenuated the antifibrotic effect of DA-GIP. In heart failure rats, DA-GIP reduced myocardial fibrosis, chamber dilatation, and systolic dysfunction. DA-GIP suppresses cardiac fibroblast activity through Akt-dependent eNOS activation and subsequent NO production, thereby improving cardiac remodeling and function in experimental heart failure.
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6. Rebalancing mitochondrial dynamics restores succinate dehydrogenase activity and reduces succinate release in hepatocellular carcinoma.
6. 重建线粒体动力学可恢复肝细胞癌中的琥珀酸脱氢酶活性并减少琥珀酸释放PMID:日期:2026-08-27Dysregulated mitochondrial dynamics in cancer cells perturbs mitochondrial function and metabolism and promotes cancer progression. Its impacts on the electron transport chain, oxidative phosphorylation, redox balance, and glycolysis are well recognized. However, its influence on tricarboxylic acid (TCA) cycle activity is less clear. In this study, we hypothesized that excessive mitochondrial fragmentation suppresses the expression of succinate dehydrogenase (SDH), resulting in the accumulation and secretion of succinate. We tested this hypothesis in human hepatocellular carcinoma (HCC) cell model, murine xenograft tumor model, human HCC tumor tissues, and serum samples from patients with HCC. Genetic suppression and pharmacological inhibition of dynamin-related protein 1 (Drp1) were employed to examine their effects on SDH expression and succinate levels. The effects of Mdivi-1, a pharmacological inhibitor of Drp1-mediated mitochondrial fission, were evaluated in the xenograft tumor model, and the impact of succinate on mitochondrial dynamics was assessed in Huh7 cells. The results reveal imbalance of mitochondrial fission and fusion proteins and increase in mitochondrial fragmentation which was associated with reduced expression of SDH and increased succinate. Succinate dehydrogenase B subunit (SDHB) mRNA levels were reduced in human HCC tumor tissues, and higher SDHB expression was associated with improved overall and relapse-free survival. Serum succinate levels were increased in patients with HCC. Genetic suppression and pharmacological inhibition of Drp1 resulted in restoration of SDH and reduction of succinate. Administration of Mdivi-1 reduced tumor growth and lung metastasis in the xenograft tumor model, which was associated with reduced p-Drp1 and increased SDHB. Addition of succinate to Huh7 cells enhanced Drp1-mediated mitochondrial fragmentation while succinate antibodies abrogated it. Overexpression of SDHB in Huh7 cells suppressed Drp1 activation and mitochondrial fragmentation through reduction of succinate. By contrast, SDHB silencing with SDHB siRNA enhanced Drp1 activation and mitochondrial fragmentation. These results suggest a positive feedback regulation of mitochondrial fragmentation by SDH/succinate. These findings indicate that the mitochondrial fragmentation-SDH-succinate regulatory loop plays an important role in HCC growth and metastasis and may represent a potential target for new drug development.
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7. Editorial expression of concern: Trypsin-induced proteome alteration during cell subculture in mammalian cells.
7. 编辑关注声明：胰蛋白酶在哺乳动物细胞传代过程中诱导的蛋白质组改变PMID:日期:2026-08-24该文献暂无摘要。
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8. NOX2 deficiency exacerbates lupus nephritis through activation of NLRP3 inflammasome in neutrophils.
8. NOX2缺陷通过激活中性粒细胞中的NLRP3炎症小体加重狼疮性肾炎PMID:日期:2026-08-19Lupus nephritis (LN) is a severe manifestation of systemic lupus erythematosus (SLE) associated with significant morbidity. Although reduced production of reactive oxygen species (ROS) by neutrophils correlates with severe SLE, the specific mechanisms linking ROS deficiency to heightened renal inflammation remain unknown. We aimed to elucidate the role of NOX2-derived ROS in LN pathogenesis and identify potential therapeutic targets. We conducted an in vivo study using a pristane-induced lupus model in Ncf1 (NOX2-deficient) mice and wild-type controls. We assessed LN severity and characterized renal immune infiltration using flow cytometry and single-cell RNA sequencing (scRNA-seq). We performed transcriptomic analysis to evaluate the function of NOX2-deficient neutrophils. Finally, we tested the therapeutic efficacy of an IL-1 receptor antagonist in ameliorating disease severity in the NOX2-deficient mice. NOX2 deficiency exacerbated LN severity compared to wild-type controls, demonstrated by increased serum anti-dsDNA antibody titers and worsened LN scores. Through scRNA-seq, we identified a distinct, activated neutrophil subset in Ncf1 mice featuring a robust interferon signature and high Nlrp3 expression. Transcriptomic analysis confirmed the upregulation of core NLRP3 pathway within these cells. Crucially, treating NOX2-deficient mice with an IL-1 receptor antagonist reduced LN activity scores. Our results showed that NOX2 deficiency was associated with the expansion of a highly inflammatory renal neutrophil subset that may contribute to aggravated renal inflammation. These findings suggest that NOX2 functions as a negative regulator of the NLRP3 inflammasome and IL-1β blockade represents a promising precision therapeutic strategy for patients with LN who exhibit impaired ROS production.
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9. Safety and antiviral activity of inhaled siRNA SNS812 for treatment of mild-to-moderate COVID-19: a phase 2 randomized trial.
9. 吸入siRNA SNS812治疗轻度至中度新冠肺炎的安全性和抗病毒活性：2期随机试验PMID:日期:2026-08-14SARS-CoV-2 remains a global health threat because ongoing viral evolution and immune evasion reduce the effectiveness of existing therapies. SNS812 is an inhaled small interfering RNA targeting a highly conserved region of the viral RNA-dependent RNA polymerase gene, representing a strategy that may enable broader antiviral activity against emerging variants. In this phase 2, double-blind, randomised, placebo-controlled trial, adults with mild-to-moderate COVID-19 within 3 days of symptom onset were randomly assigned (1:1:1) to receive placebo or inhaled SNS812 (100 mg or 200 mg) once daily for 7 days (ClinicalTrials.gov identifier: NCT05941793). Safety was the primary endpoint. Secondary endpoints included the time to sustained alleviation (TTSA) and resolution (TTSR) for prespecified composite target symptoms and individual symptoms. Virological outcomes were exploratory. A total of 135 participants were enrolled, with more than 90% infected with immune-evasive SARS-CoV-2 variants. No treatment-related adverse events or serious adverse events were reported. In exploratory analyses, the 200 mg SNS812 group showed a shorter median time to SARS-CoV-2 antigen negativity (2.9 vs 3.6 days; p = 0.007) and a faster viral load reduction rate (- 0.755 vs - 0.652; p = 0.040), demonstrating dose-dependent virological effects. In the modified intention-to-treat population, exploratory symptom analyses showed shorter TTSA and TTSR for prespecified target symptoms with SNS812 200 mg compared with placebo (median TTSR 6.1 vs 8.1 days; adjusted hazard ratio 2.07, 95% CI 1.30-3.29; median TTSA 3.6 vs 6.5 days; adjusted hazard ratio 1.81, 95% CI 1.14-2.88). Inhaled SNS812 was safe and well tolerated and showed dose-dependent antiviral activity, with exploratory signals of symptomatic improvement in adults with mild-to-moderate COVID-19 infected with immune-evasive variants. These findings support further evaluation in larger, adequately powered trials, including older and higher-risk populations.
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10. The ZBTB16/CUL3/ROC1 ubiquitin ligase drives the degradation of pathogenic pendrin (SLC26A4) protein variants.
10. ZBTB16/CUL3/ROC1泛素连接酶驱动致病性pendrin（SLC26A4）蛋白变体的降解PMID:日期:2026-08-13Pathogenic sequence alterations in the SLC26A4 gene, which encodes the solute carrier SLC26A4/pendrin, lead to Pendred syndrome and non-syndromic autosomal recessive deafness type B4 (DFNB4), two of the most common forms of hearing loss worldwide. Many pathogenic SLC26A4 protein variants exhibit reduced cellular levels due to ubiquitin-proteasome system (UPS)-mediated degradation, and UPS inhibition rescues their plasma membrane expression and ion transport function. However, the underlying molecular mechanisms remain unclear and may involve interactions with novel molecular partners. A candidate SLC26A4 protein partner was found by a yeast two-hybrid screening. The biological significance of this interaction has been studied by immunohistochemistry and co-localization in the mouse inner ear and kidney, co-immunoprecipitation of endogenous and recombinant proteins, Liquid Chromatography-Tandem Mass Spectrometry, and Fluorescence Resonance Energy Transfer. We identified the zinc finger and BTB domain-containing protein ZBTB16 as a novel SLC26A4-interacting partner. ZBTB16 co-localized with SLC26A4 in the outer sulcus and spiral prominence epithelial cells of the mouse cochlea and in the apical membrane of non-alpha non-beta intercalated cells of the distal nephron. ZBTB16 was found to be part of a ubiquitin-ligase complex comprising the scaffold protein Cullin 3 and the ubiquitin ligase RocI, and to bind with its C-terminal zinc finger region a unique amino acid sequence within the C-terminal Sulfate Transporter and Anti-Sigma factor Antagonist (STAS) domain of SLC26A4. This direct molecular interaction leads to increased site- and variant-specific ubiquitination and accelerated degradation of SLC26A4. Finally, using AI-based structure prediction, we provide an atomistic model of the complete SLC26A4/ZBTB16/Cullin 3/RocI complex in agreement with our experimental results. These findings describe a primary mechanism of SLC26A4 regulation in the inner ear and kidney and of SLC26A4 loss of function in Pendred syndrome and deafness DFNB4, and identify potential novel molecular targets for therapeutic intervention.