BIOSCIENCE REPORTS生物科学报告

BIOSCIENCE REPORTS(英文缩写 BIOSCIENCE REP),ISSN 0144-8463,eISSN 1573-4935,中文译名:生物科学报告 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。

2026 年数据 · 影响因子
4.500
JCR 分区
Q2
CAS 分区
B3
近一年发文量
154
本站 PubMed 收录统计

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。

ISSN: 0144-8463 · eISSN: 1573-4935 · 缩写: BIOSCIENCE REP ·中文: 生物科学报告

期刊介绍

选择期刊介绍栏目

期刊简介

Bioscience Reports 是一本覆盖分子与细胞生命科学多个领域的开放获取期刊,发表基础与转化研究。其内容涉及细胞信号、代谢、基因调控、蛋白质功能及疾病机制等方向,读者主要为高校、科研院所从事生物医学研究的科研人员与研究生。期刊强调机制性发现与实验数据的可靠性,在生物化学与分子生物学领域具有一定国际能见度。

研究方向

主要接收分子生物学、细胞生物学、生物化学及相关交叉学科的研究论文,主题包括信号转导、基因表达调控、蛋白质结构与功能、代谢调控、肿瘤与炎症机制等。论文类型以原创研究为主,也接受综述和方法学报道,鼓励提供机制解释和可重复的实验证据。

期刊特色

研究取向偏重实验机制与功能验证,论文通常要求较完整的体外或体内证据链。写作上强调数据呈现清晰、统计规范、结论与结果匹配。适合已有较扎实实验基础、希望在国际生物医学读者群中传播机制性发现的作者,也适合关注细胞与分子过程的研究生参考。

投稿难度

投稿难度中等偏上,对机制新颖性和数据完整性有一定要求,但并非仅以分区判断。建议在投稿前明确科学问题、补足关键对照与重复实验,规范统计与图像数据,并针对审稿人可能质疑的机制环节准备补充材料。语言表达和图表质量也需达到国际期刊基本水准。

历年影响因子趋势

JCR 数据年份影响因子JCR 分区
20213.977Q3
20224.000Q2
20233.800Q2
20244.700Q1
20254.500Q2

BIOSCIENCE REPORTS 最新收录文献

  1. JCR分区: Q2 CAS分区: B3 影响因子: 4.5

    1. A Thermally Processed Cafeteria Diet Reproducibly Mimics Early Metabolic Syndrome Through Obesogenic, Inflammatory, and Adipose Dysfunctions in Wistar Rats.

    作者:
    Susana Barbosa Ribeiro, Rômulo Camilo de Oliveira Melo, Lucas Vinicius Souza de Carvalho, Arnóbio Antônio da Silva Júnior, Raimundo Fernandes de Araújo Júnior, Amanda Silveira da Silva, Gabrielle Marques de Paiva, Vinicius Barreto Garcia, Ana Heloneida de Araújo Morais, Ana Júlia Felipe Camelo Aguiar, Caroline Addison Carvalho Xavier de Medeiros, Maiara De Morais, Bruna Rafaela Martins Dos Santos, Rafael Lino Mokwa, Francisco Canindé de Souza Júnior, Maíra Conceição Jerônimo de Souza Lima, Ciro Dantas Soares, Aurigena Antunes de Araújo
    日期:
    2026-10-02

    The obesogenic nutrient composition and processing characteristics of ultra-processed foods may contribute to metabolic dysfunction. This study evaluated a standardized cafeteria diet, alone or combined with low-dose streptozotocin (STZ), in male Wistar rats. Animals (n = 32) were allocated to Healthy Control, STZ (35 mg/kg), Cafeteria Diet (CAF), and CAF+STZ groups. The diet contained standard chow, condensed milk, refined sugar, hydrogenated fat, soybean oil, and chocolate-filled biscuits, homogenized and thermally processed at 180 °C. After 102 days, anthropometric, metabolic, inflammatory, gene expression, microbiota, and histopathological parameters were assessed. CAF induced a marked obesogenic phenotype, with increased body weight (+172.3%) and abdominal circumference (+38.7%; p < 0.01). CAF showed hyperglycemia (median glucose, 403 mg/dL) and higher HOMA-IR than Healthy Control (p < 0.01); CAF+STZ also showed increased HOMA-IR (p < 0.05). CAF increased IL-1β and IL-6 (p < 0.05), triglycerides, adipocyte hypertrophy (p < 0.01), and adipose Leptin expression (p < 0.05), while reducing muscle Slc2a4/GLUT4 expression (p < 0.01). Liver, kidney, and pancreatic histopathological scores did not differ significantly. Gut microbiota showed marked compositional imbalance and low taxonomic evenness, with Firmicutes (99.83%), Ligilactobacillus (99.36%), and Lactobacillaceae (99.52%) predominating, while Enterobacteriaceae represented 0.14%. Despite no reduction in Shannon or Simpson indices, extreme Ligilactobacillus dominance indicated a restricted and uneven community. Overall, the cafeteria diet reproduced obesity-associated metabolic dysfunction, characterized by hyperglycemia, insulin resistance, inflammation, adipocyte hypertrophy, altered glucose and leptin expression, and substantial microbiota restructuring.

  2. JCR分区: Q2 CAS分区: B3 影响因子: 4.5

    2. MUC17 and the intestinal glycocalyx: structure, regulation, and barrier function in health and disease.

    2. MUC17与肠道糖萼:在健康与疾病中的结构、调控及屏障功能
    作者:
    Fleur Claire van de Koolwijk, Thaher Pelaseyed
    日期:
    2026-10-01

    The intestinal epithelial surface is protected by a multilayered barrier system that includes secreted mucus and a membrane-bound glycocalyx. While gel-forming mucins have been extensively studied, the transmembrane mucins that form the enterocyte glycocalyx remain less well understood. MUC17 has emerged as a dominant and functionally important transmembrane mucin of the small intestinal brush border, where its large, extensively O-glycosylated extracellular domain forms a dense, hydrated barrier between luminal microbes and the epithelial membrane. This review summarizes current knowledge of MUC17 biology, from genomic organization and protein architecture to glycosylation, trafficking, developmental regulation, and barrier function. Particular emphasis is placed on how MUC17 contributes to size-selective exclusion, bacterial segregation, and host-microbe homeostasis. This review further discusses the developmental establishment of the MUC17-rich enterocyte glycocalyx during the suckling-weaning transition and covers the mechanisms that regulate MUC17 localization and dynamics in epithelial cells, including apical targeting, membrane retention, recycling, turnover, and responses to inflammatory cues. Finally, the review examines the consequences of altered MUC17 expression or function, with particular emphasis on glycocalyx barrier defects, host-microbe interactions, bacterial access to the epithelium, and the relevance of MUC17 dysfunction to Crohn's disease and experimental models of intestinal infection. Together, the review positions MUC17 as a central structural and functional component of the intestinal glycocalyx and an underexplored therapeutic axis for restoring epithelial barrier integrity in intestinal disease.

  3. JCR分区: Q2 CAS分区: B3 影响因子: 4.5

    3. Characterization of the Mos10 (Vps60) ESCRT-III complex.

    作者:
    Joël Vollmar, Thomas Brune, Ralf Kölling
    日期:
    2026-09-28

    The endosomal sorting complex required for transport (ESCRT)-III protein Mos10 (also known as Vps60) forms an alternative ESCRT-III complex in yeast. Here, we explored the relationship between the Mos10 complex and the classical Snf7-based complex. Both proteins could in principle form completely independent complexes or mixed complexes. To address the present issue, we examined the composition of ESCRT-III in different mutants of the endosomal protein sorting pathway by co-immunoprecipitation. We found that the formation of the Mos10 complex was dependent on the activity of the AAA+ ATPase Vps4. At the same time, loss of Vps4 activity led to an accumulation of the canonical ESCRT-III proteins Snf7, Vps2, and Vps24. In none of the mutants tested could a complex be detected that contains only Mos10 and no Snf7. We therefore favor the view that Snf7 and Mos10 form mixed complexes, which could play a role in the disassembly of ESCRT-III. To further dissect the interactions among the ESCRT-III subunits, Mos10 mutants were isolated. The L49P mutation in helix α1 altered Mos10 localization, while the L150P mutation in helix α4 abolished membrane association. A potential explanation for the effect of the L49P mutation on Mos10 function is suggested by AlphaFold modeling.

  4. JCR分区: Q2 CAS分区: B3 影响因子: 4.5

    4. High-resolution cryoEM of nucleosomes in nuclear extracts of mammalian cells.

    作者:
    De-Sheng Ker, Hedaya Aboalnaga, Luca Pellegrini
    日期:
    2026-09-24

    Frontier Structural Biology methods are transitioning from analysis of reconstituted macromolecular complexes in vitro to imaging of macromolecular assemblies within the physiological confines of the cell. Preparation of samples for in situ cryoEM analysis requires FIB milling or ultramicrotome sectioning, laborious and technically challenging procedures that are low-throughput and require a high degree of technical skills. We have devised a simple approach for cryoEM of nuclear macromolecular complexes that preserves to a high degree their physiological environment while removing the need for thin sectioning of the sample. The method requires only the preparation of nuclear extracts without additional purification or enrichment steps. We applied the method to obtain a 2.3 Å cryoEM structure of nucleosomes visualised directly in the nuclear lysate of human cells.

  5. JCR分区: Q2 CAS分区: B3 影响因子: 4.5

    5. The convergent roles of metabolic dysfunction, alcohol, and iron in steatotic liver disease: a review.

    作者:
    Afolabi Akanbi, Kim Bridle, Darrell H G Crawford
    日期:
    2026-09-24

    Steatotic liver disease (SLD) encompasses a broad spectrum of disorders influenced by metabolic dysfunction, alcohol use, and other cofactors. The updated classification of metabolic dysfunction-associated steatotic liver disease (MASLD) and alcohol-associated liver disease (ALD), along with the recognition of the overlapping entity MetALD, allows for better identification of patients at increased risk of progressive liver injury. While iron dysregulation is known to worsen both MASLD and ALD, its role within MetALD remains poorly defined. Understanding how iron contributes to this combined phenotype may provide new insight into why these patients experience more severe disease outcomes. This review synthesises current evidence linking iron to MASLD, ALD, and their intersection in MetALD. It introduces the concept of Fe-MetALD, a "triple-hit" phenotype where metabolic dysfunction, alcohol, and iron overload act together to accelerate liver injury. Mechanistically, these insults share common pathways involving oxidative stress, mitochondrial dysfunction, endoplasmic reticulum stress, inflammation, and hepatic stellate cell activation, collectively promoting fibrosis progression and potentially increasing the risk of cirrhosis and hepatocellular carcinoma. Experimental studies suggest that the combination of these insults produces more severe liver injury than any individual factor alone. Emerging therapies that target iron pathways, including hepcidin mimetics, ferroportin inhibitors, and iron-reduction strategies like venesection or chelation, may offer therapeutic potential, although current evidence remains largely preclinical. Recognising Fe-MetALD as a high-risk phenotype supports incorporating iron markers into diagnosis and developing therapies targeting metabolic, alcohol-related, and iron-mediated injury. Understanding this triple-hit interaction may improve risk stratification and guide future therapies for SLD.

  6. JCR分区: Q2 CAS分区: B3 影响因子: 4.5

    6. Metataxonomic strategy to decipher gut bacteriome biomarkers of type 2 diabetes and obesity in Tunisian population.

    作者:
    Meriem Fassatoui, Thierry Pedron, Nadia Kheriji, Meriem Hechmi, Hamza Dallali, Haifa Jmel, Henda Jamoussi, Abdelmajid Abid, Philippe J Sansonetti, Rym Kefi
    日期:
    2026-09-23

    Metabolic disorders are multifactorial diseases and major global health concerns, with many individuals worldwide responding inadequately to treatments. The gut bacteriome regulates metabolism and offers therapeutic potential; however, research from North Africa remains scarce despite the growing prevalence of non-communicable diseases in the region. This study examines gut bacterial profiles of Tunisian type 2 diabetic (T2D), obese (OB), and non-diabetic (ND) individuals within the framework of personalized medicine. Ninety-five participants were enrolled (33 ND, 26 T2D, 26 T2D with obesity and cardiovascular complications (T2D_OBCV), and 10 OB). Bacterial 16S rDNA V3-V4 regions were sequenced on Illumina MiSeq and analyzed using the QIIME 2 pipeline. Obese subjects exhibited gut dysbiosis with lower Akkermansia (p = 0.02) and Ligilactobacillus (p = 0.04) levels, an enrichment of Bifidobacterium (p = 0.004), as well as Sutterella (p = 0.03) and Erysipelatoclostridium (p = 0.02). However, the gut bacteriome landscape of T2D patients reveals differences in the distribution of Shigella (p = 0.01) highly abundant in the intestine, and a depletion of Clostridia vadin BB 60 group (p = 0.02) and Oscillospiraceae UCG 005 (p = 0.01). Noting that the gut bacteriome of T2D_OBCV patients is characterized by a depletion of Asteroleplasma (p = 0.01), Oscillospiraceae UCG 005 ( p = 0.02), Eubacterium ruminantium group (p= 0,0007), and Romboutsia (p = 0.002) beside an enrichment of Fusicatenibacter (p = 0.02). Gut bacteriome alterations in Tunisian T2D and obese subjects may serve as metabolic biomarkers.

  7. JCR分区: Q2 CAS分区: B3 影响因子: 4.5
  8. JCR分区: Q2 CAS分区: B3 影响因子: 4.5

    8. Balancing inflammation under stress: glucocorticoid regulation of innate immune pathways.

    作者:
    Kirsten M Kenney, Sabrina S Burgener
    日期:
    2026-09-22

    Despite our constant exposure to potential dangers, our ability to withstand infection and tissue damage relies on a network of coordinated cellular security systems. One of these security features is our innate immune system, which senses danger signals from invading pathogens as well as host-derived stress signals while remaining largely unresponsive to normal host molecules and the flora of the host microbiota. This intertwining network of cellular guardians expresses pattern recognition receptors to recognise specifically pathogen-associated molecular patterns and danger-associated molecular patterns and elicit an inflammatory response. Inflammation is an integral process to eliminate a pathogenic threat while simultaneously promoting tissue repair. However, a balance exists, and persistent or aberrant inflammation can instead drive tissue damage and disease. To douse inflammatory flames, the endocrine system releases endogenous glucocorticoids, which possess potent immunomodulatory actions. This review will explore the cross-talk between endogenous glucocorticoid signalling and innate immune signalling pathways.

  9. JCR分区: Q2 CAS分区: B3 影响因子: 4.5

    9. The membrane skeleton density of red blood cells in MYH9-related disease patients is decreased.

    作者:
    Shaopeng Sun, Jiabin Pan, Ning Zhang, Xianghong Jin, Tie-Nan Zhu, Zhijie Kang, Jihong Hao, Xiang-Dong Li
    日期:
    2026-09-17

    MYH9-related disease (MYH9-RD) is a rare autosomal dominant disorder caused by mutations in MYH9 gene, which encodes the heavy chain of nonmuscle myosin IIA. Nearly all MYH9-RD patients present with macrothrombocytopenia, characterized by decreased platelet count and increased platelet size. In the present study, we collected blood samples from three MYH9-RD patients (R702S, D1424N, and R1464C) and unexpectedly found that the actin levels in the red blood cells (RBCs) from all three MYH9-RD patients are substantially lower than the healthy controls. We further revealed that the levels of two RBC membrane skeleton proteins, α-spectrin and tropomodulin, are also reduced in MYH9-RD RBCs. We showed that the membrane skeleton of MYH9-RD RBCs was more porous and that MYH9-RD RBCs produced more severe deformation under hyperosmotic pressure compared with healthy controls. We propose that defects in the membrane-skeleton network of RBCs may be an abnormal manifestation of MYH9-RD.

  10. JCR分区: Q2 CAS分区: B3 影响因子: 4.5

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