Acta biochimica et biophysica Sinica最新文献_第6页

Smc3-dependent chromatin insulation prevents transcriptional inversion at the Wnt-responsive Wisp1/ Ndrg1 locus in mouse ESCs. smc3依赖性染色质绝缘可阻止小鼠ESCs中wnt响应Wisp1/ Ndrg1位点的转录反转。

IF 4.5 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2026-08-20 DOI: 10.3724/abbs.2026144

Lu Fang, Ce Xu, Peng Yang

引用次数: 0

Myricetin-functionalized Prussian blue nanoparticles enable multi-modal therapy against methicillin-resistant Staphylococcus aureus and accelerate wound repair. 杨梅素功能化的普鲁士蓝纳米颗粒能够多模式治疗耐甲氧西林金黄色葡萄球菌，并加速伤口修复。

IF 4.5 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2026-08-19 DOI: 10.3724/abbs.2026150

Song Xiang, Wen Zheng, Xiaohe Zhang, Jing Zhang, Shicheng Zhang, Jiaxing Li, Shengkai Li, Xuedan Yu, Chunlin Zhang, Guzhen Cui, Zhenghong Chen, Li Lei

{"title":"Myricetin-functionalized Prussian blue nanoparticles enable multi-modal therapy against methicillin-resistant Staphylococcus aureus and accelerate wound repair.","authors":"Song Xiang, Wen Zheng, Xiaohe Zhang, Jing Zhang, Shicheng Zhang, Jiaxing Li, Shengkai Li, Xuedan Yu, Chunlin Zhang, Guzhen Cui, Zhenghong Chen, Li Lei","doi":"10.3724/abbs.2026150","DOIUrl":"https://doi.org/10.3724/abbs.2026150","url":null,"abstract":"Traditional photothermal antibacterial therapy is limited by a narrow therapeutic window. Here, myricetin-functionalized Prussian blue analog nanoparticles (M@HPBA) are developed as a multimodal platform for methicillin-resistant Staphylococcus aureus (MRSA) infection and wound repair. Doping with cobalt, zinc, and copper enhances photothermal conversion and enzyme-mimetic activities. Under near-infrared irradiation, localized heating induces bacterial damage and triggers the controlled release of metal ions and myricetin. Released myricetin scavenges excess reactive oxygen species, alleviating oxidative stress and inflammation to promote healing. In vitro, M@HPBA with irradiation achieves high antibacterial efficiency against MRSA. In a murine wound infection model, this strategy markedly reduces bacterial burden and accelerates tissue regeneration, with a wound closure rate significantly higher than controls. Transcriptomic analysis reveals that M@HPBA regulates inflammatory and antioxidant pathways in MRSA-infected wounds, enhancing susceptibility to photothermal and ROS/metal ion killing. M@HPBA demonstrates broad-spectrum antibacterial activity and favorable biosafety. These findings establish a synergistic strategy integrating photothermal therapy, nanozyme catalysis, ion release, and antioxidant intervention, providing a translatable paradigm for precision antimicrobial therapy and infected wound management.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148786931","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Pannexin 1 drives cardiac fibroblast activation and fibrosis via the ATP-purinergic receptor-JAK2/STAT3 axis in heart failure. Pannexin 1在心力衰竭中通过atp -嘌呤能受体- jak2 /STAT3轴驱动心脏成纤维细胞活化和纤维化。

IF 4.5 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2026-08-19 DOI: 10.3724/abbs.2026147

Lieyang Qin, Yunjing Zhang, Diyaerjiang Aierken, Zexu Wang, Wen Zhang, Jiayu Zheng, Chen Liu

{"title":"Pannexin 1 drives cardiac fibroblast activation and fibrosis via the ATP-purinergic receptor-JAK2/STAT3 axis in heart failure.","authors":"Lieyang Qin, Yunjing Zhang, Diyaerjiang Aierken, Zexu Wang, Wen Zhang, Jiayu Zheng, Chen Liu","doi":"10.3724/abbs.2026147","DOIUrl":"https://doi.org/10.3724/abbs.2026147","url":null,"abstract":"Pannexin 1 (PANX1), a member of the gap junction protein family, is ubiquitously expressed across various tissues and plays a key role in ATP release and signal transduction. In this study, we investigate Panx1 expression in cardiac fibroblasts under pathological conditions, specifically focusing on heart failure. Transcriptomic analysis reveals that Panx1 expression is upregulated in mouse hearts after transverse aortic constriction (TAC) surgery. Single-cell sequencing data from TAC mice indicate that Panx1 is predominantly expressed in fibroblasts, and its expression is significantly elevated in TAC mice. The upregulation of the PANX1 protein in fibroblasts following TAC is further corroborated by immunofluorescence staining and western blot analysis. Similarly, single-cell sequencing data from human heart failure patients are consistent with those from TAC mice, showing high PANX1 expression in fibroblasts. Pathway enrichment analysis of fibroblasts with differential Panx1 expression reveals that the JAK/STAT signaling pathway is commonly enriched in both species. In vitro knockdown and overexpression of the Panx1 gene are used to demonstrate its effect on the fibroblast phenotype. In vivo injection of a PANX1 blocker provides evidence for the role of Panx1 in alleviating cardiac fibrosis. The PANX1 channel is expressed in cardiac fibroblasts and is upregulated after TAC. Bioinformatics analysis suggests that this process is associated with the JAK/STAT signaling pathway. The Panx1 gene regulates phenotypic changes in fibroblasts and activates the downstream JAK/STAT signaling pathway via the ATP-purinergic receptor.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148786873","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

PBLD promotes virus-induced pyroptosis via NF-κB/Caspase-3/GSDME signaling pathway. PBLD通过NF-κB/Caspase-3/GSDME信号通路促进病毒诱导的焦亡。

IF 4.5 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2026-08-19 DOI: 10.3724/abbs.2026133

Hongchao Zhu, Xiaonan Sun, Zixuan Gao, Haojing Wu, Rui Li, Jiyu Zhang, Peili Hou, Hongmei Wang, Hongbin He

{"title":"PBLD promotes virus-induced pyroptosis via NF-κB/Caspase-3/GSDME signaling pathway.","authors":"Hongchao Zhu, Xiaonan Sun, Zixuan Gao, Haojing Wu, Rui Li, Jiyu Zhang, Peili Hou, Hongmei Wang, Hongbin He","doi":"10.3724/abbs.2026133","DOIUrl":"https://doi.org/10.3724/abbs.2026133","url":null,"abstract":"Phenazine biosynthesis-like domain-containing protein (PBLD) has been proven to be a critical regulator of tumor suppression and antiviral innate immunity; however, its role in pyroptosis remains unexplored. Our current investigation shows that PBLD promotes pyroptosis in bovine parainfluenza virus 3 (BPIV3)- or herpes simplex virus type 1 (HSV-1)-triggered HeLa cells, along with BPIV3- or bovine ephemeral fever virus (BEFV)-infected BHK-21 cells, as manifested by increased hallmark features of pyroptosis, including cell swelling, plasma membrane disintegration, elevated lactate dehydrogenase (LDH) release, and reduced cell survival. Further studies reveal that PBLD facilitates virus-induced pyroptosis mediated by GSDME N-terminal cleavage but independent of GSDMD cleavage. Using caspase-specific inhibitors and knockout cell lines, we identify Caspase-3, but not Caspase-8, as essential for virus-induced GSDME-dependent pyroptosis. Mechanistically, PBLD enhances Caspase-3 activation by upregulating PUMA mRNA levels via the NF-κB signaling pathway. Furthermore, silencing of NF-κB abolishes PBLD-induced PUMA upregulation and Caspase-3 and GSDME cleavage. In summary, these findings reveal that PBLD potentiates virus-triggered pyroptosis through the NF-κB/PUMA/Caspase-3/GSDME signaling pathway. This investigation provides unprecedented understanding of the molecular mechanisms by which PBLD regulates cell death and highlights its promise as a pharmacological target for viral infections and inflammatory diseases.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148786878","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Diabetes mellitus aggravates sepsis-induced lung injury by triggering NPM3-ACSL1 pathway-mediated ferroptosis. 糖尿病通过触发NPM3-ACSL1途径介导的铁下垂加重败血症诱导的肺损伤。

IF 4.5 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2026-08-19 DOI: 10.3724/abbs.2026149

Zhuang Yu, Hongjiao Xu, Yanlin Han, Yu Zhou, Jun Zhu, Haoran Liu, Jihong Jiang, Jinbao Li, Minmin Zhu

{"title":"Diabetes mellitus aggravates sepsis-induced lung injury by triggering NPM3-ACSL1 pathway-mediated ferroptosis.","authors":"Zhuang Yu, Hongjiao Xu, Yanlin Han, Yu Zhou, Jun Zhu, Haoran Liu, Jihong Jiang, Jinbao Li, Minmin Zhu","doi":"10.3724/abbs.2026149","DOIUrl":"https://doi.org/10.3724/abbs.2026149","url":null,"abstract":"Hyperglycemia is a poor prognostic factor in critically ill septic patients with diabetes. Acute lung injury (ALI) resulting from hyperglycemia combined with sepsis remains an urgent clinical challenge. However, the mechanisms by which hyperglycemia contributes to sepsis-associated ALI remain unclear. In this study, we investigate the molecular mechanisms through which hyperglycemia accelerates ALI and mortality in sepsis using in vivo and in vitro models. High NPM3 expression not only mediates H3K18la levels but also promotes its binding to the ACSL1 promoter. Elevated ACSL1 expression and abnormal subcellular organelle localization disrupt lipid metabolism in macrophages, ultimately leading to ferroptosis. Our findings indicate that hyperglycemia enhances ferroptosis via the NPM3-H3K18la-ACSL1 axis in macrophages during sepsis-associated ALI. Targeted inhibition of this axis effectively suppresses hyperglycemia-induced ferroptosis in macrophages and reduces ALI and mortality in septic mice. Thus, targeting the NPM3-H3K18la-ACSL1 axis represents a promising therapeutic strategy for hyperglycemic/diabetic patients with sepsis-associated ALI.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148786783","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

lncRNA Pvt1 promotes retinal ischemia-reperfusion injury by modulating the PPM1B/RIPK3 pathway through promoter methylation. lncRNA Pvt1通过启动子甲基化调控PPM1B/RIPK3通路，促进视网膜缺血再灌注损伤。

IF 4.5 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2026-08-17 DOI: 10.3724/abbs.2026100

Xiaojing Xia, Qiyu Chen, Zeyu Cheng, Wenqi Hu, Yun Tan, Nan Qing, Jiaqi Liu, Kai Huang, Bo Hu, Lei Shang

{"title":"lncRNA Pvt1 promotes retinal ischemia-reperfusion injury by modulating the PPM1B/RIPK3 pathway through promoter methylation.","authors":"Xiaojing Xia, Qiyu Chen, Zeyu Cheng, Wenqi Hu, Yun Tan, Nan Qing, Jiaqi Liu, Kai Huang, Bo Hu, Lei Shang","doi":"10.3724/abbs.2026100","DOIUrl":"https://doi.org/10.3724/abbs.2026100","url":null,"abstract":"Retinal ischemia-reperfusion (I/R), a hallmark feature of many retinal degenerative diseases, often leads to irreversible neuronal damage. Among the various forms of cell death, necroptosis has emerged as a pivotal mechanism contributing to retinal neurodegeneration. Here, we identify a novel regulatory axis that modulates neuronal necroptosis using the long non-coding RNA (lncRNA) Pvt1. Using both in vitro (R28 cell line) and in vivo (intravitreal injection of adeno-associated virus carrying lncRNA Pvt1 shRNA in rats) models, the role of lncRNA Pvt1 under I/R in vivo and oxygen-glucose deprivation/reperfusion (OGD/R) in vitro is assessed. Comprehensive molecular and cellular analyses show that I/R or OGD/R induce robust necroptotic responses in neuronal cells. Notably, lncRNA Pvt1 knockdown significantly alleviates these necroptotic phenotypes by inhibiting RIPK3 phosphorylation. Mechanistically, lncRNA Pvt1 knockdown reduces Ppm1b promoter methylation, restoring PPM1B expression. Subsequently, PPM1B protein upregulation facilitates RIPK3 dephosphorylation, effectively dampening the necroptosis signaling cascade. These findings reveal that the previously unrecognized lncRNA Pvt1/PPM1B/p-RIPK3 axis is essential for neuronal survival following ischemic stress. This study provides compelling evidence that targeting the lncRNA Pvt1 is a promising therapeutic strategy for mitigating retinal neuronal necroptosis. Modulating this pathway provides new opportunities for the treatment of I/R-related retinal diseases.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-08-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148786925","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Immune regulation by hypothermia: from triggers and mechanisms to therapeutic applications. 低温的免疫调节：从触发和机制到治疗应用。

IF 4.5 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2026-08-11 DOI: 10.3724/abbs.2026142

Xingchao Pan, Yangyue Ni, Xiang Li, Jianfeng Chen

引用次数: 0

Structure and enzymatic properties of human retroviral-like aspartic protease 1 and functional roles of disease-associated mutations. 人逆转录病毒样天冬氨酸蛋白酶1的结构和酶特性及疾病相关突变的功能作用

IF 4.5 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2026-08-11 DOI: 10.3724/abbs.2026141

Xueqian Feng, Ziyue Chen, Chao Lan, Jianping Ding

{"title":"Structure and enzymatic properties of human retroviral-like aspartic protease 1 and functional roles of disease-associated mutations.","authors":"Xueqian Feng, Ziyue Chen, Chao Lan, Jianping Ding","doi":"10.3724/abbs.2026141","DOIUrl":"https://doi.org/10.3724/abbs.2026141","url":null,"abstract":"The establishment of the epidermal barrier is essential for terrestrial vertebrate survival. Retroviral-like aspartic protease 1 (ASPRV1), also known as skin aspartic protease (SASPase), plays a central role in this process by facilitating the initial cleavage of profilaggrin into filaggrin monomers, which is vital for skin hydration and barrier integrity. Mutations disrupting this activity are linked to hereditary skin disorders. Evolutionarily, ASPRV1 originated from the domestication of an ancient retroviral sequence and comprises a Gag-like domain and a C-terminal protease domain. While it shares structural similarity with HIV-1 protease (HIV-1 PR), the molecular basis for its unique enzymatic properties and substrate specificity remains unclear. Here, we present the biochemical characterization and crystal structures of mature human ASPRV1 (ASPRV1-14) in multiple states, including wild-type, catalytically inactive mutants bound to self-cleavage and filaggrin peptides, and a complex with the HIV-1 PR inhibitor indinavir. Our results demonstrate that ASPRV1-14 exhibits an ionic strength-dependent monomer-dimer equilibrium, shifting from a low-activity monomer at low ionic strength to a high-activity dimer at high ionic strength. Structural analysis reveals that ASPRV1-14 possesses distinctly hydrophobic S2/S2' pockets, dictating a strict requirement for hydrophobic residues at the P2/P2' positions of substrates and explaining its resistance to most HIV-1 PR inhibitors, except indinavir. Furthermore, analysis of disease-associated mutations indicates two main pathogenic mechanisms: disrupting the S2/S2' pocket ( e. g., V243A) or interfering with the self-cleavage maturation process ( e. g., I186T, K199E, R311C/P, and P314T). Collectively, these findings provide a comprehensive molecular framework for understanding the roles of ASPRV1 in epidermal homeostasis and the pathogenesis of skin diseases, offering insights for future therapeutic development.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148757458","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

7-Dehydrocholesterol-mediated ferroptosis is governed by glucose availability in pancreatic ductal adenocarcinoma. 7-脱氢胆固醇介导的铁下垂是由胰腺导管腺癌的葡萄糖可用性控制的。

IF 4.5 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2026-08-10 DOI: 10.3724/abbs.2026106

Xiaojun Ren, Yaqiong Zhang, Xiaoxuan Zhou, Saijun Xiao, Kai Huang, Yingjie Dai, Xunjun Yang, Hezhi Fang, Jianxin Lyu, Zhengquan Yang, Minghua Jiang

{"title":"7-Dehydrocholesterol-mediated ferroptosis is governed by glucose availability in pancreatic ductal adenocarcinoma.","authors":"Xiaojun Ren, Yaqiong Zhang, Xiaoxuan Zhou, Saijun Xiao, Kai Huang, Yingjie Dai, Xunjun Yang, Hezhi Fang, Jianxin Lyu, Zhengquan Yang, Minghua Jiang","doi":"10.3724/abbs.2026106","DOIUrl":"10.3724/abbs.2026106","url":null,"abstract":"7-Dehydrocholesterol (7-DHC) has recently emerged as an endogenous suppressor of lipid peroxidation/ferroptosis; however, its function in nutrient-poor microenvironments remains undefined. Here, we demonstrate that activated c-Myc directly occupies the DHCR7 promoter in pancreatic ductal adenocarcinoma (PDAC) cells, transcriptionally upregulating DHCR7, which converts 7-DHC into cholesterol, thereby fuelling PDAC cell proliferation. Under glucose deprivation, DHCR7 deletion triggers pronounced ferroptosis in PDAC cells, an effect that is sharply attenuated when glucose is supplemented. Mechanistically, DHCR7 inhibition drives 7-DHC accumulation, which plays a dual role: it traps free radicals (anti-ferroptosis) and yet simultaneously depletes the antioxidant pool (pro-ferroptosis), with the net outcome dictated by glucose availability. The antioxidant pool maintained by glucose is required to counteract the pro-peroxidation effects of 7-DHC; once glucose is limited, the radical-trapping-mediated anti-ferroptosis function of 7-DHC becomes negligible. Furthermore, glucose restriction in vitro and a low-glucose diet in vivo both sensitized PDAC cells to DHCR7 inhibition-triggered lipid peroxidation, which allows accelerated cell death or suppressed tumor growth. Collectively, 7-DHC, negatively regulated by the c-Myc/DHCR7 axis, promotes lipid peroxidation and ferroptosis in glucose-deficient PDAC tumors, revealing a metabolic vulnerability that can be exploited for therapy.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148719465","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

P-selectin binds to complement C4B in human blood plasma. p -选择素与人血浆中的补体C4B结合。

IF 4.5 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2026-08-10 DOI: 10.3724/abbs.2026131

Yangyang Wang, Zheng Zhang, Hailiang Hu, Zhezhe Qu, Paul W R Harris, Ju Liu

引用次数: 0