Biochemical and biophysical research communications最新文献

{"title":"Enhanced STIM1 expression drives platelet hyperactivity in diabetes","authors":"Haoxuan Zhong ,&nbsp;Maieryemu Waresi ,&nbsp;Xu Jia ,&nbsp;Junbo Ge","doi":"10.1016/j.bbrc.2025.151510","DOIUrl":"10.1016/j.bbrc.2025.151510","url":null,"abstract":"<div><div>Stromal interaction molecule 1 (STIM1), a key regulator of calcium signaling located in the endoplasmic reticulum, is crucial for platelet function. While elevated STIM1 expression is observed in platelets from diabetic patients, its role in diabetes-induced platelet hyperreactivity remains unclear. In this study, we found a positive correlation between STIM1 expression and agonist-induced platelet aggregation in platelets from patients with type 2 diabetes mellitus (T2DM). Platelets with high STIM1 expression exhibited enhanced aggregation, P-selectin release, integrin αIIbβ3 activation, spreading, and clot retraction compared to those with low STIM1 expression. Similar findings were observed in db/db mice. Furthermore, the store-operated calcium entry channel inhibitor CM4620 demonstrated superior antiplatelet and antithrombotic efficacy compared to aspirin in both db/db mice and patients with T2DM. Our results suggest that elevated STIM1 expression contributes to enhanced platelet reactivity in diabetes, and targeting STIM1 may offer a promising novel therapeutic approach for thrombosis prevention in this patient population.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"753 ","pages":"Article 151510"},"PeriodicalIF":2.5,"publicationDate":"2025-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143465247","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The evaluation of the effects of metformin on the rat testes at a light and electron microscopic level","authors":"Selin Ursavas ,&nbsp;Yurdun Kuyucu ,&nbsp;Ebru Dundar Yenilmez ,&nbsp;Abdullah Tuli ,&nbsp;Muhammetnur Tekayev ,&nbsp;Ufuk O. Mete","doi":"10.1016/j.bbrc.2025.151507","DOIUrl":"10.1016/j.bbrc.2025.151507","url":null,"abstract":"<div><div>The present study aimed to assess the histological and ultrastructural changes in the testes induced by metformin. Eighteen adult male Wistar rats were divided into three groups: a control group, a low-dose metformin group, and a high-dose metformin group. Following thirty days of metformin administration, blood samples, and testes tissues were collected and subjected to biochemical, histological, and ultrastructural analyses. In the groups treated with metformin, degenerative changes were observed, including irregular seminiferous tubules, disruption of epithelial integrity, a decrease in spermatogenic cells, and dilated intercellular spaces. These changes were evident in both the light and electron microscopic evaluations, and the severity varied depending on the metformin dosage. The findings showed that the diameter of the seminiferous epithelium and epithelium height decreased significantly in the high-dose group. Also, Follicle-stimulating hormone (FSH), Luteinizing hormone (LH), and testosterone levels altered significantly, with increased levels of all hormones observed in the high-dose metformin-administered group than in the control group. For the markers of oxidative stress and antioxidant status respectively there were no significant differences observed in the levels of Malondialdehyde (MDA) between the groups, however, Superoxide dismutase (SOD) activity significantly decreased in the high-dose metformin-administered group compared to the control group.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"753 ","pages":"Article 151507"},"PeriodicalIF":2.5,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143453901","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"HDAC6 deficiency aggravates ductular reactions through aggresome-mediated hepatocyte apoptosis","authors":"Shanshan Tan ,&nbsp;Guoquan Fu ,&nbsp;Yixia Xie ,&nbsp;Xueying Xie ,&nbsp;Junyan Yan ,&nbsp;Lifang Jin","doi":"10.1016/j.bbrc.2025.151511","DOIUrl":"10.1016/j.bbrc.2025.151511","url":null,"abstract":"<div><div>Ductular reactions (DRs) contribute significantly to the occurrence and development of liver disease. While histone deacetylase 6 (HDAC6) is known to regulate injury repair in multiple tissues, its exact role in DRs remains unclear. This study examined the role and underlying mechanism of HDAC6 in DRs using an HDAC6 knockout (HDAC6^−/y) male mouse model. Wild type and HDAC6-deficient male mice were administered 3,5 diethoxicarbonyl-1,4 dihydrocollidine (DDC) to induce DRs. The impact of HDAC6 inhibition on aggresome formation was assessed <em>in vitro</em> using AML-12 hepatocytes exposed to H₂O₂ and treated with tubastatin A (TSA), a selective HDAC6 inhibitor. Fluorescence immunohistochemistry and quantitative real-time polymerase chain reaction (qRT-PCR) were employed to quantify protein and gene expression levels, respectively. Immunohistochemical and qRT-PCR analyses revealed that HDAC6 deficiency exacerbated DRs and fibrosis, accompanied by increased expression of transforming growth factor β (TGF-β) and activation of the Notch signaling pathway. Additionally, genetic knockout or pharmacological inhibition of HDAC6 promoted hepatocyte apoptosis <em>in vivo</em> and <em>in vitro</em>, as evidenced by elevated <em>caspase3</em>, <em>caspase9</em>, and <em>p53</em> expression. Furthermore, TSA treatment induced the formation of aggresomes in H₂O₂-exposed AML-12 hepatocytes, which were encased by vimentin filaments. These findings demonstrate that HDAC6 deficiency promotes DRs and liver fibrosis through the formation of intracellular aggregates, ultimately leading to hepatocyte apoptosis.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"753 ","pages":"Article 151511"},"PeriodicalIF":2.5,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143453900","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Development of a reverse genetic system for mononegaviruses using a circular polymerase extension reaction","authors":"Masaaki Nakashima ,&nbsp;Keiko Funabiki ,&nbsp;Satoko Izume ,&nbsp;Yuki Maruyama ,&nbsp;Atsuko Yamamoto ,&nbsp;Michie Watanabe ,&nbsp;Saori Okaga ,&nbsp;Takashi Hashimoto ,&nbsp;Yoko Hayasaki-Kajiwara ,&nbsp;Yoshiyuki Nakano","doi":"10.1016/j.bbrc.2025.151493","DOIUrl":"10.1016/j.bbrc.2025.151493","url":null,"abstract":"<div><div>Reverse genetic systems are commonly used to study viruses; the ability to rapidly generate recombinant viruses is critical for studying the functions of viral genes and for the development of new interventions, such as antivirals or vaccines. Reverse genetic methods for mononegaviruses, viruses with non-segmented negative-strand RNA genomes, commonly incorporate a full-length viral genome cDNA into a bacterial artificial chromosomes (BACs) or plasmid DNA. However, the large size of mononegavirus genomes makes their manipulation challenging. In this study, to overcome this limitation, we adopted and optimized the circular polymerase extension reaction (CPER) method for mononegavirus reverse genetics. We segmented the genome of the mononegavirus, respiratory syncytial virus (RSV), into approximately 1.2–2.5 kb fragments and reassembled them with a linker fragment containing a T7 promotor into a circular full-length viral cDNA. Recombinant RSV was then generated by co-transfecting cells with the circular cDNA and helper plasmids carrying viral proteins that are essential to initiate viral replication. This reverse genetic system has the potential to be applied to other mononegaviruses.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"754 ","pages":"Article 151493"},"PeriodicalIF":2.5,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143479879","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Radioprotection and enhanced efficacy by curcumin-loaded chitosan nanoparticles in mitigating radiation-induced liver injury","authors":"Rasool Azmoonfar ,&nbsp;Masoud Moslehi ,&nbsp;Daryoush Shahbazi-Gahrouei ,&nbsp;Elham Shiri ,&nbsp;Mehdi Azizi","doi":"10.1016/j.bbrc.2025.151512","DOIUrl":"10.1016/j.bbrc.2025.151512","url":null,"abstract":"<div><h3>Introduction</h3><div>This study aimed to evaluate the protective effect of curcumin-loaded chitosan nanoparticles (Cur-CsNPs) against radiation-induced liver damage in rats. Curcumin's antioxidant and anti-inflammatory properties, combined with chitosan's drug delivery potential, were leveraged to mitigate the harmful effects of ionizing radiation (IR) on the liver.</div></div><div><h3>Methods</h3><div>Cur-CsNPs were characterized using TEM, XRD, DLS, and FTIR. Spectrophotometry assessed drug loading and curcumin release. Cytotoxicity was evaluated using MTT assay on HepG2 cells. The experimental design involved eight groups: a control group, three groups receiving different doses of Cur-CsNPs (25, 50, 100 mg/kg), three groups receiving the same doses plus irradiation (6Gy), and one group receiving irradiation only. H&amp;E and MTC staining were used for histopathological evaluation. The activity of liver enzymes ALT, AST, ALP, and GGT was measured.</div></div><div><h3>Results</h3><div>In this study, three types of Cur-CsNPs were synthesized using varying ratios of chitosan to TPP ratios, resulting in average sizes of 660 nm, 230 nm, and 120 nm. Cur-CsNPs which exhibited the highest encapsulation efficiency, was selected for further evaluation. TEM confirmed its spherical shape with an average size of 37 nm. Drug release studies demonstrated an 85 % release at pH 5.4 within 70 h. MTT assays indicated low cytotoxicity, with high cell viability maintained across all concentrations and time points. Liver enzyme analysis in rats revealed that Cur-CsNPs, particularly when combined with radiation, mitigated radiation-induced liver damage. Histological examination showed that treatment with Cur-CsNPs reduced liver damage, inflammation, necrosis, and fibrosis in irradiated groups compared to the radiation-only group, which exhibited severe liver damage.</div></div><div><h3>Conclusion</h3><div>The findings of this study show that Cur-CsNPs possess significant potential as a therapeutic agent for protecting against radiation-induced liver injury. The favorable drug release profile, low cytotoxicity, and protective effects observed in enzyme levels and histological assessments highlight the efficacy of Cur-CsNPs. The findings imply that Cur-CsNPs could be an effective strategy for enhancing liver protection in radiation exposure scenarios, warranting further investigation into their mechanisms of action and potential clinical applications<strong>.</strong></div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"753 ","pages":"Article 151512"},"PeriodicalIF":2.5,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143453825","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mitochondrial targeted therapies in MAFLD","authors":"Sien Lai,&nbsp;Dongsheng Tang,&nbsp;Juan Feng","doi":"10.1016/j.bbrc.2025.151498","DOIUrl":"10.1016/j.bbrc.2025.151498","url":null,"abstract":"<div><div>Metabolic dysfunction-associated fatty liver disease (MAFLD) is a clinical-pathological syndrome primarily characterized by excessive accumulation of fat in hepatocytes, independent of alcohol consumption and other well-established hepatotoxic agents. Mitochondrial dysfunction is widely acknowledged as a pivotal factor in the pathogenesis of various diseases, including cardiovascular diseases, cancer, neurodegenerative disorders, and metabolic diseases such as obesity and obesity-associated MAFLD. Mitochondria are dynamic cellular organelles capable of modifying their functions and structures to accommodate the metabolic demands of cells. In the context of MAFLD, the excess production of reactive oxygen species induces oxidative stress, leading to mitochondrial dysfunction, which subsequently promotes metabolic disorders, fat accumulation, and the infiltration of inflammatory cells in liver and adipose tissue. This review aims to systematically analyze the role of mitochondria-targeted therapies in MAFLD, evaluate current therapeutic strategies, and explore future directions in this rapidly evolving field. We specifically focus on the molecular mechanisms underlying mitochondrial dysfunction, emerging therapeutic approaches, and their clinical implications. This is of significant importance for the development of new therapeutic approaches for these metabolic disorders.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"753 ","pages":"Article 151498"},"PeriodicalIF":2.5,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143453826","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Zinc ions trigger the prion protein liquid-liquid phase separation","authors":"Mariana Juliani do Amaral ,&nbsp;Letícia Soares de Oliveira,&nbsp;Yraima Cordeiro","doi":"10.1016/j.bbrc.2025.151489","DOIUrl":"10.1016/j.bbrc.2025.151489","url":null,"abstract":"<div><div>Prion diseases are characterized by the misfolding and conversion of the monomeric prion protein (PrP) to a multimeric aggregated pathogenic form, known as PrP^Sc. We and others have recently shown that biomolecular condensates formed via liquid-liquid phase separation of PrP can undergo maturation to solid-like species that resemble pathological aggregates, and this process is modulated by DNA, RNA, and oxidative conditions. Conversely, the most well-studied ligand of PrP, copper ions, induce liquid-like condensates of PrP that accumulate Cu²⁺ <em>in vitro</em>, and live PrP^C-expressing cells show condensation at the cell surface as triggered by physiologically relevant conditions of Cu²⁺ and protein concentrations. Since PrP can also bind to Zn²⁺ through its intrinsically disordered N-terminal domain, though with different affinities and binding modes than Cu²⁺, we hypothesized that Zn²⁺ could modulate PrP phase separation differently from copper ions. Using an appropriate buffer with negligible metal ion binding, as well as relevant pH, ionic strength, molecular crowding, and Zn²⁺ concentrations, we show that recombinant PrP undergoes phase separation with Zn²⁺. <span>Furthermore</span>, we show that metal ion-induced condensation of PrP is dependent on the N-terminal domain (residues 23–90). <em>In vitro</em> Fluorescence Recovery After Photobleaching (FRAP) experiments and thioflavin T aggregation kinetics support key differences in the molecular properties of PrP:Zn²⁺ <em>versus</em> PrP:Cu²⁺ phase separated states. FRAP analysis indicated that both Cu²⁺ and Zn²⁺ promote liquid-like PrP condensates; however, PrP:Zn²⁺condensates exhibit a faster recovery. Cu²⁺ pronouncedly inhibits seed-induced PrP misfolding, whereas Zn²⁺ provides a milder delay in PrP aggregation. Our findings provide insights on Zn²⁺-induced phase separation of PrP, supporting a variety of previously proposed functions of PrP in metal sequestering and uptake, processes that could be effectively regulated through biomolecular condensation.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"753 ","pages":"Article 151489"},"PeriodicalIF":2.5,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143445804","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The miR-22–5p/Clec4e axis has diagnostic potential in fructose-induced nonalcoholic fatty liver disease","authors":"Haidong He ,&nbsp;Yifan Zhu ,&nbsp;Xiaoguo Ji ,&nbsp;Suying Pu ,&nbsp;Hui Zheng","doi":"10.1016/j.bbrc.2025.151496","DOIUrl":"10.1016/j.bbrc.2025.151496","url":null,"abstract":"<div><div>Nonalcoholic fatty liver disease (NAFLD) is significantly influenced by microRNAs in its development and progression. This study aimed to identify microRNA profiles and RNA regulatory networks for NAFLD intervention. Mice were fed a high-fructose diet (HFrD) to induce NAFLD. Small RNA-seq and mRNA-seq were used to analyze liver microRNA and mRNA profiles of HFrD-fed versus normal chow-fed (Chow) mice. The differentially expressed genes (DEGs) and miRNAs (DE-miRNAs) were identified, followed by enrichment analysis. A protein‒protein interaction network of overlapping DEGs and DE-miRNA targets was constructed, along with a competing endogenous RNA (ceRNA) network. Mendelian randomization (MR) was performed to verify the causal relationship between top DEGs and NAFLD. The study identified 13 DE-miRNAs and 854 DEGs in the liver between HFrD mice and Chow mice. A Venn diagram revealed that 58 of the predicted target genes of the 13 DE-miRNAs were shared with the DEGs. Finally, 6 DE-miRNAs, 34 DEGs, and 20 predicted lncRNAs were selected to construct the ceRNA regulatory network. The upregulated DEG Clec4e, a target gene of miR-22–5p, was significantly correlated with the risk of NAFLD (OR: 1.41, 95 % CI: 1.04–1.92, <em>P</em> = 0.029) in the MR analysis, and RT-qPCR was applied to validate Clec4e expression in the livers of HFrD mice. Further, the dual-luciferase reporter assay confirmed that miR-22–5p could directly inhibit Clec4e expression by targeting its 3′-UTR. This study identified several novel miRNAs and genes as potential biomarkers of NAFLD. In particular, the miR-22–5p/Clec4e axis is a potential diagnostic target for NAFLD.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"753 ","pages":"Article 151496"},"PeriodicalIF":2.5,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143445803","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TPD52 (isoform 3) promotes resistance to mTOR-targeted inhibitors by regulating c-Myc, PTEN, and direct activation of 4E-BP1 in LNCaP androgen-dependent cells","authors":"Priyanka Khilar ,&nbsp;Ramesh Ummanni","doi":"10.1016/j.bbrc.2025.151495","DOIUrl":"10.1016/j.bbrc.2025.151495","url":null,"abstract":"<div><div>A therapeutic strategy targeting the PI3K–AKT–mTOR pathway is widely seen as promising against prostate cancer (PCa) treatment. However, resistance to targeted inhibitors is still a major challenge. Herein we observed that the overexpression of TPD52 (isoform 3) in LNCaP, PCa cells confers resistance to mTOR inhibitors, specifically everolimus and rapamycin. This study demonstrates that TPD52 promotes the proliferation and survival of tumor cells treated with mTOR inhibitors by hyperactivating PI3K/AKT. Despite the inactivation of downstream targets like p70S6K and S6 upon mTOR inhibition, p4E-BP1 remained consistently high in TPD52 overexpressing LNCaP cells, suggesting activation of an alternative regulatory mechanism independent of mTOR. Furthermore, elevated c-Myc levels were correlated with overexpression of TPD52 and were linked to loss of PTEN expression further promoting drug resistance. Contrarily, silencing of TPD52 and c-Myc sensitized LNCaP cells to mTOR inhibitors by restoring PTEN levels and further downregulation of 4E-BP1. Above all, downregulation of both TPD52 and c-Myc enhanced the sensitivity of LNCaP-TPD52 cells facilitating apoptosis indicating a potential strategy to overcome resistance to mTOR inhibitors in PCa. Taken together, these findings underscore the role of TPD52 through c-Myc in conferring resistance to mTOR inhibitors and warrant further exploration of their molecular mechanisms in PCa treatment.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"753 ","pages":"Article 151495"},"PeriodicalIF":2.5,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143445805","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A mini review on the regulation of coagulation homeostasis through interfering with vitamin K-dependent coagula-tion/anticoagulation factors","authors":"Jiangbo Tong ,&nbsp;Yuan Zhao ,&nbsp;Yongchao Jin ,&nbsp;Zhenyu Hao ,&nbsp;Shixin Li ,&nbsp;Mei Sun","doi":"10.1016/j.bbrc.2025.151494","DOIUrl":"10.1016/j.bbrc.2025.151494","url":null,"abstract":"<div><div>Coagulation disorders, such as excessive bleeding or thrombosis, present significant health challenges. Vitamin K-dependent proteins (VKDPs), including coagulation and anticoagulation factors, are essential for maintaining the coagulation homeostasis due to their key roles in the coagulation cascade. Therefore, VKDPs have become significant targets for regulating coagulation homeostasis, and various strategies have been developed, primarily including small molecule drugs and nanomaterials. This review presents the summary of these strategies, focusing on the mechanisms, effectiveness and limitations. It first discusses the pivotal role of VKDPs in the coagulation cascade, followed by an in-depth analysis of how small molecule drugs and nanomaterials to regulate hemostasis through interfering with VKDPs. Furthermore, this review addresses the challenges faced in the current approaches and potential future research directions. We hope this review will contribute to advancing the development of novel methods for modulating coagulation homeostasis through VKDP interference.</div></div>","PeriodicalId":8779,"journal":{"name":"Biochemical and biophysical research communications","volume":"753 ","pages":"Article 151494"},"PeriodicalIF":2.5,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143437453","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}