截止目前，引用Bioss產(chǎn)品發(fā)表的文獻共35,336篇，總影響因子176,219.79分，發(fā)表在Nature, Science, Cell以及Immunity等頂級期刊的文獻共126篇，合作單位覆蓋了清華、北大、復旦、華盛頓大學、麻省理工學院、東京大學以及紐約大學等上百所國際研究機構(gòu)。
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本文主要分享11篇IF＞16的文獻，它們引用了Bioss產(chǎn)品，分別發(fā)表在CELL、Nature Biomedical Engineering、Advanced Fiber Materials、Nature Metabolism、Bioactive Materials、Advanced Functional Materials、ACS Nano期刊上，讓我們一起學習吧。

CELL [IF=42.5]

文獻引用產(chǎn)品：

bs-0297P | Human IgG | IF

作者單位：首都醫(yī)科大學宣武醫(yī)院

摘要：Exercise has well-established health benefits, yet its molecular underpinnings remain incompletely understood. We conducted an integrated multi-omics analysis to compare the effects of acute vs. long-term exercise in healthy males. Acute exercise induced transient responses, whereas repeated exercise triggered adaptive changes, notably reducing cellular senescence and inflammation and enhancing betaine metabolism. Exercise-driven betaine enrichment, partly mediated by renal biosynthesis, exerts geroprotective effects and rescues age-related health decline in mice. Betaine binds to and inhibits TANK-binding kinase 1(TBK1), retarding the kinetics of aging. These findings systematically elucidate the molecular benefits of exercise and position betaine as an exercise mimetic for healthy aging.

作者單位：北京大學

文獻引用產(chǎn)品：

bs-6313R | 4 Hydroxynonenal Rabbit pAb | IHC

摘要：Increased reactive oxygen species(ROS) levels are a hallmark of inflammatory bowel disease(IBD) and constitute a major mechanism of epithelial cell death. Approaches to broadly inhibit ROS have had limited efficacy in treating IBD. Here we show that lipid peroxidation contributes to the pathophysiology of IBD by promoting ferroptosis, an iron-dependent form of programmed cell death. Mechanistically, we provide evidence of heterocellular crosstalk between intestinal fibroblasts and epithelial cells. In IBD tissues and mouse models of chronic colitis, acyl-CoA synthetase long-chain family 4(ACSL4) is overexpressed in fibroblasts. ACSL4 in fibroblasts reprograms lipid metabolism and mediates intestinal epithelial cell sensitivity to ferroptosis. In mouse models, overexpressing ACSL4 in fibroblasts results in increased intestinal epithelial ferroptosis and worsened colitis, while pharmacological inhibition or deletion of fibroblast ACSL4 ameliorates colitis. Our work provides a targeted approach to therapeutic antioxidant treatments for IBD.

文獻引用產(chǎn)品：

bsm-33112M | CD41/ITGA2B Mouse mAb | WB

文獻引用產(chǎn)品：

bs-10900R | GAPDH Rabbit pAb, Loading Control | WB

作者單位：中山大學

摘要：The ligamentization process of the tendon graft in anterior cruciate ligament(ACL) reconstruction is crucial for graft healing quality, thereby affecting knee joint function. Excessive scar tissue, caused by activation of trans-differentiation of fibroblasts to myofibroblasts, rather than orientated collagen fibers with normal composition and structure in the graft mid-substance seriously impacts ligamentization. The elucidation of the underlying mechanism behind the graft fibrosis may facilitate modulation of tendon graft ligamentization. Here, we show that transforming growth factor beta 1(TGF-β1) was significantly upregulated with ligamentization process, contributing to fibroblast to myofibroblast trans-differentiation and thereby leading to impaired collagen orientation with overproduction of collagen type III. Of note, we verified that prostaglandin E2(PGE2), a principal mediator of inflammation secreted by macrophages, significantly reversed TGF-β1-induced trans-differentiation of fibroblasts to myofibroblasts. Importantly, magnesium(Mg) ions were found to upregulate PGE2 production in macrophages, ultimately favoring inhibition of scar tissue formation and promoting expression of ligament-like phenotype in the graft mid-substance in rats. Consistently, the rats, with injection of the sodium alginate containing Mg ions into knee joint cavity, exhibited significantly improved gait performance and failure load relative to the control group. These results demonstrate the feasibility of using Mg ions to modulate tendon ligamentization in patients after ACL reconstruction.

Advanced Functional 

Materials [IF=19]

文獻引用產(chǎn)品：

bsm-60761R | CD206 Recombinant Rabbit mAb | IF

作者單位：同濟大學

摘要：Optimal healing of diabetic chronic wound requires a well-organized cascade integration of bacterial death, cell migration and proliferation, and extracellular remodeling. However, such biological progress is usually impaired in chronic diabetic wound and traditional antibacterial hydrogels unmatched for ordered repair needs. Herein, an iron-coordinated glycopeptide hydrogel(Fe-GP gel) that could effectively treat MRSA-infected chronic diabetic wounds within 11 days by reprogramming healing process is developed. This Fe-GP hydrogel is formed based on glucomannan-decorated peptide nanofibers framework and then loaded with tannic acid/Fe nanocomplexes. The burst release of nanocomplexes is achieved to conduct the first healing stage, which could induce the ferroptosis-like death of methicillin-resistant Staphylococcus aureus (MRSA) for eliminating over 98% of MRSA bacteria by metabolism disrupting within 6 h. In the second healing stage, sustained release of glucomannan promotes M2 macrophage polarization(five times higher than control group) through extracellular signal-regulated kinase and signal transducer and activator of transcription 6(ERK/STAT6) pathway within 2 days. After the elimination of MRSA and restoration of immune microenvironment, the remaining 3D peptide nanofibers framework is able to facilitate extracellular remodeling through anchoring fibroblast cells as the third healing stage within weeks. Overall, this glycopeptide hydrogel has demonstrated a promising approach to realize the orderly progression during healing process for enhanced treatment of drug-resistant bacteria-infected chronic wounds.

Advanced Functional 

Materials [IF=19]

文獻引用產(chǎn)品：

bs-0061R | beta-Actin Rabbit pAb, Loading Control | WB

作者單位：AIR FORCE MEDICAL CENTER, PLA

摘要：Monoclonal antibodies demonstrate significant potential in the clinical management of Human Epidermal Growth Factor Receptor 2/Estrogen Receptor-positive(HER2/ER+) breast cancer. However, the therapeutic outcomes of antitumor drugs are significantly hampered by challenges such as inter-pathway crosstalk, the restricted efficacy of single-pathway mechanisms, and suboptimal drug targeting. Herein, this study developed a Zr/Fe bimetallic MOF loaded with Cyclin-dependent kinases 4 and 6(CDK4/6) inhibitor ribociclib and surface-functionalized with trastuzumab (Herceptin). Under the acidic tumor microenvironment(TME), this nanomaterial degrades, releasing trastuzumab, ribociclib, and Fe³⁺. Trastuzumab enhances tumor targeting, reduces normal tissue toxicity, and inhibits Cyclin D1-CDK4/6 activation to decrease retinoblastoma(RB) phosphorylation, while ribociclib suppresses CDK4/6 enzymatic activity, synergistically blocking RB phosphorylation, inducing G1-phase arrest, and halting tumor proliferation. Additionally, Fe³⁺ catalyzes the conversion of H₂O₂ into highly cytotoxic hydroxyl radicals (·OH) through the Fenton reaction, leading to oxidative stress-induced cellular damage. Together, these three components synergistically inhibit the proliferation of HER2/ER+ breast cancer cells by disrupting cell cycle progression and cellular homeostasis. In vivo studies demonstrated that Zr-Fe MOF@Ribociclib@Herceptin(ZFRH) not only significantly inhibits the growth of orthotopic tumors but also effectively suppresses the formation of lung-metastatic tumors. These findings suggest a promising strategy for the precision-targeted therapy of HER2/ER+ breast cancer.

ACS Nano [IF=16]

作者單位：中國科學院武漢病毒研究

作者單位：東南大學