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截至目前，引用Bioss產(chǎn)品發(fā)表的文獻(xiàn)共37,172篇，總影響因子187,859.41分，發(fā)表在Nature, Science, Cell, Cancer Cell以及Immunity等頂刊的文獻(xiàn)共130篇，合作單位覆蓋了清華、北大、復(fù)旦、華盛頓大學(xué)、麻省理工學(xué)院、東京大學(xué)以及紐約大學(xué)等上百所國際研究機(jī)構(gòu)。
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本文主要分享10篇IF≥20的文獻(xiàn)，它們引用了Bioss產(chǎn)品，分別發(fā)表在iMeta、Advanced Materials、Bioactive Materials、Circulation Research期刊上，讓我們一起學(xué)習(xí)吧。
文獻(xiàn)引用產(chǎn)品：
bs-1226R | GPA33 Rabbit pAb | WB
bs-2489R | CD9 Rabbit pAb | WB
bs-6934R | CD81 Rabbit pAb | WB
bsm-52746R | TSG101 Recombinant Rabbit mAb | WB
bs-3614R | PPAR alpha Rabbit pAb | IF
bs-34023R | ZO-1 Rabbit pAb | IF, WB
作者單位：廣西大學(xué)
摘要：Metabolic-associated fatty liver disease (MAFLD) has become increasingly widespread. The intestine is the primary site of lipid absorption and is important for the homeostasis of lipid metabolism. However, the mechanism underlying the participation of the intestinal tract in the development of MAFLD requires additional investigation. In this study, analysis of the single-cell transcriptome of intestinal tissue from cynomolgus monkeys found that hepatic leukemia factor (HLF) participated in the genetic regulation of intestinal lipid absorption. Results obtained from normal and intestine-specific Hlf-knockout mice confirmed that HLF alleviated intestinal barrier disorders by inhibiting peroxisome proliferator-activated receptor alpha (PPARα) expression. The HLF/PPARα axis alleviated MAFLD by mediating gut microbiota-derived extracellular vesicles (fEVs), thereby inhibiting hepatocyte ferroptosis. Lipidomics and functional experiments verified that taurochenodeoxycholic acid (TCDCA), a conjugated bile acid contained in the fEVs, had a key role in the process. In conclusion, intestinal HLF activity was mediated by fEVs and identified as a novel therapeutic target for MAFLD.
Advanced Materials [IF=27.4]
文獻(xiàn)引用產(chǎn)品：
bsm-30276A-PE | mouse CD206 Rat mAb, PE conjugate | IF, FC
bs-20633R | HMGB1 Rabbit pAb | IF
bsm-30151H-PerCp-Cy5.5 | Mouse CD3e Hamster mAb, PerCp-Cy5.5 conjugated | FC
bs-0647R-FITC | CD4 Rabbit pAb, FITC conjugated | IF, FC
bsm-30396A-PE | mouse CD8a Rat mAb, PE conjugate | IF, FC
bsm-2508R-FITC | CD11c Rabbit pAb, FITC conjugated | FC
bs-1035R-APC | CD86 Rabbit pAb, APC conjugated | FC
bs-2211R-PerCP-Cy5.5 | CD80 Rabbit pAb, PerCP-Cy5.5 conjugated | FC
bsm-54156R-APC | CD11b Recombinant Rabbit mAb, APC conjugated | Other
bsm-41204R-PerCP-Cy5.5 | ADGRE1 Recombinant Rabbit mAb, PerCP-Cy5.5 conjugated | Other
作者單位：哈爾濱工程大學(xué)
摘要：Low efficacy of immunotherapy due to the poor immunogenicity of most tumors and their insufficient infiltration by immune cells highlights the importance of inducing immunogenic cell death and activating immune system for achieving better treatment outcomes. Herein, ferroelectric Bi2CuO4 nanoparticles with rich copper vacancies (named BCO-VCu) are rationally designed and engineered for ferroelectricity-enhanced apoptosis, cuproptosis, and the subsequently evoked immunotherapy. In this structure, the suppressed recombination of the electron–hole pairs by the vacancies and the band bending by the ferroelectric polarization lead to high catalytic activity, triggering reactive oxygen species bursts and inducing apoptosis. The cell fragments produced by apoptosis serve as antigens to activate T cells. Moreover, due to the generated charge by the ferroelectric catalysis, this nanomedicine can act as “a smart switch" to open the cell membrane, promote nanomaterial endocytosis, and shut down the Cu+ outflow pathway to evoke cuproptosis, and thus a strong immune response is triggered by the reduced content of adenosine triphosphate. Ribonucleic acid transcription tests reveal the pathways related to immune response activation. Thus, this study firstly demonstrates a feasible strategy for enhancing the efficacy of immunotherapy using single ferroelectric semiconductor-induced apoptosis and cuproptosis.
Advanced Materials [IF=27.4]
文獻(xiàn)引用產(chǎn)品：
作者單位：南方醫(yī)科大學(xué)
摘要：Solid nanoparticle-mediated drug delivery systems are usually confined to nanoscale due to the enhanced permeability and retention effect. However, they remain a great challenge for malignant glioma chemotherapy because of poor drug delivery efficiency and insufficient tumor penetration resulting from the blood–brain barrier/blood–brain tumor barrier (BBB/BBTB). Inspired by biological microparticles (e.g., cells) with excellent adaptive deformation, it is demonstrated that the adaptive microdrugs (even up to 3.0 µm in size) are more efficient than their nanodrugs (less than 200 nm in size) to cross BBB/BBTB and penetrate into tumor tissues, achieving highly efficient chemotherapy of malignant glioma. The distinct delivery of the adaptive microdrugs is mainly attributed to the enhanced interfacial binding and endocytosis via adaptive deformation. As expected, the obtained adaptive microdrugs exhibit enhanced accumulation, deep penetration, and cellular internalization into tumor tissues in comparison with nanodrugs, significantly improving the survival rate of glioblastoma mice. It is believed that the bioinspired adaptive microdrugs enable them to efficiently cross physiological barriers and deeply penetrate tumor tissues for drug delivery, providing an avenue for the treatment of solid tumors.
Advanced Materials [IF=27.4]
文獻(xiàn)引用產(chǎn)品：
摘要：Given the crucial role of abnormal homeostasis in tumor cells for maintaining their growth, it may be more efficient with less effort to develop anti-tumor strategies that target multiple combined mechanisms by disrupting intracellular homeostasis. Here, a copper-based nanoinducer (CGBH NNs) with multiple enzyme-like activities is designed and constructed to induce disulfidptosis-enhanced pyroptosis through disrupting multiple intracellular homeostasis for effective tumor immunotherapy. Within the tumor microenvironment (TME), CGBH NNs can disrupt intracellular glucose homeostasis and inhibit NADPH production, leading to accumulation of cystine, which further blocked the substrate and key enzyme for synthesizing glutathione. Subsequently, through cascade catalytic reactions involving enzyme activities (glutathione peroxidase-like, glucose oxidase and peroxidase-like activities), CGBH NNs can produce massive reactive oxygen species (ROS) and further disrupt intracellular redox homeostasis, resulting in the disulfidptosis-enhanced pyroptosis. The tumor cells undergoing immunogenic pyroptosis can release various cytosolic contents and inflammatory factors, eliciting robust immune responses by facilitating immune cell infiltration, and reprogramming the immunosuppressive TME. After the combination with immune checkpoint blockade therapy, CGBH NNs can effectively suppress the tumor growth and prolong the survival time of tumor-bearing mice. This work presents a novel paradigm to trigger disulfidptosis-enhanced pyroptosis by destroying intracellular homeostasis for anti-tumor immunotherapy.
Advanced Materials [IF=27.4]
文獻(xiàn)引用產(chǎn)品：
摘要：The cardiotoxicity induced by immune checkpoint inhibitors (ICIs) is associated with high mortality rates. T cells play an important role in ICI-induced cardiac injury. The inhibition of local T-cell activity is considered an effective strategy for alleviating ICI-related cardiotoxicity. Tumor-derived extracellular vesicles (EVs) contribute to immunosuppression via PD-L1 overexpression. In this study, a bioorthogonal metabolic engineering–driven EV redirecting (Biomeder) strategy for in situ engineered EVs with myocardial-targeting peptides is developed. Accumulated tumor-derived EV (TuEVs) reverses the immune environment in the heart by increasing PD-L1 levels in cardiomyocytes and/or by directly inhibiting T-cell activity. More importantly, it is found that the redirection of TuEVs further disrupts immunosuppression in tumors, which facilitates anti-tumor activity. Thus, redirecting TuEVs to the heart simultaneously enhances the antitumor efficacy and safety of ICI-based therapy. Furthermore, the Biomeder strategy is successfully expanded to prevent ICI-induced type 1 diabetes. This Biomeder technique is a universal method for the treatment of various ICI-related adverse events.
Advanced Materials [IF=26.8]
文獻(xiàn)引用產(chǎn)品：
bs-20322R | CD31 Rabbit pAb | IF
bs-33009P | Recombinant GFP protein, His | Other
作者單位：四川大學(xué)
摘要：Large-scale and deep trauma restricts the effective hemostasis and tissue regeneration management, even causing death. The formation of the fibrin network is the initial stage of wound control. Inspired by Fn's characteristics during coagulation, an artificial polycationic fibroin (pCSF/β) is designed to achieve hemostasis-regeneration transition. pCSF/β replicates the aggregation state and maturation process of Fn through intermolecular interaction and subsequent strain hardening originating from ethanol-inducing β-sheet to recapitulate natural coagulation networks, achieving mechanical reinforcement and shape recovery. Proteomics and transcriptomics analyses reveal that pCSF/β connects hemostasis and regeneration through platelet contents’ release and the PI3K/Akt signaling pathway. The results of incompressible hemostasis, large-area skin repair, and penetrating liver regeneration in animal models such as minipigs confirm pCSF/β is superior to clinical products in rapid hemostasis and synchronous tissue regeneration. The molecular design of pCSF/β provides new insights for developing biomaterials in rapid hemostasis and simultaneous regeneration.
Bioactive Materials [IF=20.3]
文獻(xiàn)引用產(chǎn)品：
作者單位：湖南大學(xué)
摘要：The expanding global population intensifies demand for sustainable protein sources. Cell-cultured meat (CM) offers a promising alternative to conventional meat production but faces challenges in scalability and food-grade scaffold design. Current scaffolds often fail to replicate muscle tissue's structural and mechanical properties or support large-scale CM production. Moreover, the sensory and nutritional qualities of CM remain understudied. Here, we developed a novel lotus fiber-based natural plant fiber (NPF) scaffold mimicking native muscle tissue architecture. Porcine muscle stem cells (pMuSCs) were cultured on the NPF scaffold (pMuSCs-NPF), and their viability, proliferation, and differentiation were evaluated. The NPF scaffolds exhibited high biocompatibility and promoted pMuSCs alignment and differentiation into organized myotubes, as evidenced by enhanced expression of myogenic markers (MYOD, MYOG, MyHC) and extracellular matrix (ECM) components (desmin, fibronectin). Multi-omics analyses revealed substantial upregulation of genes and proteins associated with muscle development and ECM remodeling in pMuSCs-NPF compared to conventional plastic culture. Sensory and nutritional analyses indicated that the resulting CM closely resembled traditional meat in appearance, texture, and nutritional profile, with comparable levels of protein and essential amino acids. Moreover, the NPF scaffold demonstrated scalability and supported adipogenic differentiation, which is vital for imparting meat-like flavor and texture. These findings establish NPF scaffolds as a viable and cost-effective platform for sustainable CM cultiv@tion.
Bioactive Materials [IF=20.3]
文獻(xiàn)引用產(chǎn)品：
作者單位：北京大學(xué)第三醫(yī)院
摘要：Craniofacial muscles are essential for a variety of functions, including fine facial expressions. Severe injuries to these muscles often lead to more devastating consequences than limb muscle injuries, resulting in the loss of critical functions such as mastication and eyelid closure, as well as facial aesthetic impairment. Therefore, the development of targeted repair strategies for craniofacial muscle injuries is crucial. In this study, we engineered an adipose-derived decellularized extracellular matrix (adECM) bioscaffold co-loaded with seed cells and bioactive factors. The seed cells were STIM1-overexpressing adipose-derived stem cells (STIM1-ASCs), which exhibit directed and highly efficient myogenic differentiation, addressing the low differentiation efficiency of conventional ASCs that limits muscle regeneration. The bioactive factor used was insulin-like growth factor-2 (IGF-2), which modulates the immune microenvironment by reprogramming mitochondrial energy metabolism to promote M2 macrophage polarization. These M2 macrophages further suppress fibroblast collagen deposition, alleviating muscle fibrosis, while simultaneously enhancing the myogenic differentiation of STIM1-ASCs and myotube formation. Together, the recellularized adECM bioscaffold harnesses these dual mechanisms (promoting functional muscle regeneration and anti-fibrotic repair) to significantly improve the recovery of volumetric muscle loss (VML) in the masseter. The development of this bifunctional bioscaffold offers a novel therapeutic strategy and theoretical foundation for treating severe craniofacial muscle injuries.
Bioactive Materials [IF=20.3]
文獻(xiàn)引用產(chǎn)品：
作者單位：吉林大學(xué)第一醫(yī)院
摘要：As one of the key targets of tumor metabolic therapy, glucose dyshomeostasis by disrupting glucose metabolism possesses the potential to reverse therapeutic resistance of a variety of regulated cell deaths (RCDs), but the functional pathways are not fully revealed and employed. Herein, we demonstrate that the intervention on SLC7A11/GSH/GPX4 antioxidant axis by glucose dyshomeostasis can simultaneously promote disulfidptosis, cuproptosis and ferroptosis, which is verified by employing glucose oxidase (GOx)-modified copper-apigenin (CuAp) network nanoshuttles (CuAp@GOx NSs) in ovarian tumor therapy. Ap and GOx can jointly induce glucose dyshomeostasis respectively by inhibiting glucose transporter 1-mediated glucose uptake upstream, and consuming massive glucose downstream. As a result of glucose dyshomeostasis, the NADPH supplement is downregulated, which further disrupts SLC7A11/GSH/GPX4 antioxidant axis. This simultaneously boosts disulfidptosis by facilitating cystine accumulation, cuproptosis by attenuating GSH-mediated Cu+ inactivation, and ferroptosis by downregulating GPX4 expression. Owing to the combination of disulfidptosis, cuproptosis and ferroptosis, CuAp@GOx NSs exhibit good efficacy in treating ovarian tumor model. This work proposes an alternative strategy for tumor therapy based on glucose dyshomeostasis, which mainly targets the RCDs relating to SLC7A11/GSH/GPX4 axis.
Circulation Research [IF=20.1]
文獻(xiàn)引用產(chǎn)品：
作者單位：廣州醫(yī)科大學(xué)附屬婦女兒童醫(yī)院
摘要：
Increasing evidence suggests that long noncoding RNAs play significant roles in vascular biology and disease development. One such long noncoding RNA, PSMB8-AS1, has been implicated in the development of tumors. Nevertheless, the precise role of PSMB8-AS1 in cardiovascular diseases, particularly atherosclerosis, has not been thoroughly elucidated. Thus, the primary aim of this investigation is to assess the influence of PSMB8-AS1 on vascular inflammation and the initiation of atherosclerosis.
We generated PSMB8-AS1 knockin and Apoe (Apolipoprotein E) knockout mice (Apoe?/?PSMB8-AS1KI) and global Apoe and proteasome subunit-β type-9 (Psmb9) double knockout mice (Apoe?/?Psmb9?/?). To explore the roles of PSMB8-AS1 and Psmb9 in atherosclerosis, we fed the mice with a Western diet for 12 weeks.
Long noncoding RNA PSMB8-AS1is significantly elevated in human atherosclerotic plaques. Strikingly,Apoe?/?PSMB8-AS1KImice exhibited increased atherosclerosis development, plaque vulnerability, and vascular inflammation compared withApoe?/?mice. Moreover, the levels of VCAM1 (vascular adhesion molecule 1) and ICAM1 (intracellular adhesion molecule 1) were significantly upregulated in atherosclerotic lesions and serum ofApoe?/?PSMB8-AS1KImice. Consistently, in vitro gain- and loss-of-function studies demonstrated thatPSMB8-AS1induced monocyte/macrophage adhesion to endothelial cells and increased VCAM1 and ICAM1 levels in a PSMB9-dependent manner. Mechanistic studies revealed thatPSMB8-AS1inducedPSMB9transcription by recruiting the transcription factor NONO (non-POU domain-containing octamer-binding protein) and binding to thePSMB9promoter. PSMB9 (proteasome subunit-β type-9) elevated VCAM1 and ICAM1 expression via the upregulation of ZEB1 (zinc finger E-box-binding homeobox 1).Psmb9deficiency decreased atherosclerotic lesion size, plaque vulnerability, and vascular inflammation inApoe?/?mice in vivo. Importantly, endothelial overexpression ofPSMB8-AS1-increased atherosclerosis and vascular inflammation were attenuated byPsmb9knockout.
PSMB8-AS1 promotes vascular inflammation and atherosclerosis via the NONO/PSMB9/ZEB1 axis. Our findings support the development of new long noncoding RNA–based strategies to counteract atherosclerotic cardiovascular disease.
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