Biochimica et biophysica acta. Molecular cell research最新文献

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PGK1 mediates glycolysis and cell proliferation in endometriosis by regulating DDIT4 nuclear translocation PGK1通过调节DDIT4核易位介导子宫内膜异位症的糖酵解和细胞增殖
IF 4.6 2区 生物学
Biochimica et biophysica acta. Molecular cell research Pub Date : 2025-06-16 DOI: 10.1016/j.bbamcr.2025.120009
Xuemei Zhang , Yadi Wang , Yujie Tang , Ran Wei, Runze Zhao, Zhenhai Yu, Chao Lu
{"title":"PGK1 mediates glycolysis and cell proliferation in endometriosis by regulating DDIT4 nuclear translocation","authors":"Xuemei Zhang ,&nbsp;Yadi Wang ,&nbsp;Yujie Tang ,&nbsp;Ran Wei,&nbsp;Runze Zhao,&nbsp;Zhenhai Yu,&nbsp;Chao Lu","doi":"10.1016/j.bbamcr.2025.120009","DOIUrl":"10.1016/j.bbamcr.2025.120009","url":null,"abstract":"<div><div>Endometriosis (EM), a gynecologic disorder affecting 10 % of childbearing age women, with complex pathogenesis involving cell proliferation and metabolic abnormalities similar to malignancies. Unusual expression of key enzymes and regulators in glycolysis pathway contributes to the development of endometriosis. Phosphoglycerate kinase 1 (PGK1) was a key enzyme in glycolysis with additional roles as a transcription factor co-activator and protein kinase. We discovered that PGK1 was elevated and associated strongly with the development of EM. The PGK1 inhibitor NG52 inhibited the growth of endometriosis lesions in mice by preventing cell migration and proliferation. Furthermore, we found that DNA damage response 4 (DDIT4) was a new downstream target gene of PGK1. PGK1 regulated the nuclear translocation of DDIT4. Additionally, we also observed that PGK1 up-regulate the transcriptional activity of DDIT4, leading to DDIT4 overexpression that promoted the development of endometriosis. These findings may provide new insights for potential non-hormonal targeted therapies for endometriosis treatment.</div></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1872 7","pages":"Article 120009"},"PeriodicalIF":4.6,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144322121","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
Mechanical stretch-mediated fibroblast activation: The pivotal role of Piezo1 channels 机械拉伸介导的成纤维细胞激活:Piezo1通道的关键作用。
IF 4.6 2区 生物学
Biochimica et biophysica acta. Molecular cell research Pub Date : 2025-06-13 DOI: 10.1016/j.bbamcr.2025.120008
Shiwei Tu , Yanwei Li , Junyi Li , Ning Ma , Kaifang Yao , Zhihan Chen , Zezhi Fan , Zhifang Xu , Yuping Sa , Peng Jia , Xiaowei Lin , Shenjun Wang , Yuxin Fang , Yangyang Liu , Yi Guo
{"title":"Mechanical stretch-mediated fibroblast activation: The pivotal role of Piezo1 channels","authors":"Shiwei Tu ,&nbsp;Yanwei Li ,&nbsp;Junyi Li ,&nbsp;Ning Ma ,&nbsp;Kaifang Yao ,&nbsp;Zhihan Chen ,&nbsp;Zezhi Fan ,&nbsp;Zhifang Xu ,&nbsp;Yuping Sa ,&nbsp;Peng Jia ,&nbsp;Xiaowei Lin ,&nbsp;Shenjun Wang ,&nbsp;Yuxin Fang ,&nbsp;Yangyang Liu ,&nbsp;Yi Guo","doi":"10.1016/j.bbamcr.2025.120008","DOIUrl":"10.1016/j.bbamcr.2025.120008","url":null,"abstract":"<div><div>Mechanical forces are crucial in regulating fibroblast behavior, yet the underlying mechanisms remain unclear. This study aims to elucidate the role of the Piezo1 ion channel in fibroblast responses to mechanical stimulation. A mechanical stimulation culture platform was developed using a polydimethylsiloxane (PDMS)-based stretchable membrane and the Cell Tank uniaxial cell stretching system. Fibroblasts subjected to uniaxial cyclic stretching were analyzed using proteomic profiling, Western blotting, and confocal laser scanning microscopy to assess cytoskeletal changes and activation markers. Immunofluorescence staining was performed to evaluate the expression of Piezo1, YAP1, and Ki67 proteins. Cell viability and migration capacity were assessed using Calcein-AM/PI double staining and a migration assay. Mechanical stretch-induced fibroblast activation is characterized by morphological changes, increased proliferation, and enhanced migration. The cytoskeletal reorganization was observed, with elevated F-actin expression. Modulating Piezo1 activity altered fibroblast activation, indicating its essential role in mechanotransduction. These findings demonstrate that mechanical stretch upregulates Piezo1 expression, promoting fibroblast activation through the YAP pathway. This study provides new insights into the mechanotransduction mechanisms in fibroblasts and highlights the critical role of Piezo1 in mediating responses to mechanical stimuli, which may have implications for understanding tissue remodeling and fibrosis.</div></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1872 7","pages":"Article 120008"},"PeriodicalIF":4.6,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144301116","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
The role of hypoxia-inducible factor-3α in human disease 缺氧诱导因子-3α在人类疾病中的作用
IF 4.6 2区 生物学
Biochimica et biophysica acta. Molecular cell research Pub Date : 2025-06-11 DOI: 10.1016/j.bbamcr.2025.120007
Alejandro López-Mejía, Paola Briseño-Díaz, Martha Robles-Flores
{"title":"The role of hypoxia-inducible factor-3α in human disease","authors":"Alejandro López-Mejía,&nbsp;Paola Briseño-Díaz,&nbsp;Martha Robles-Flores","doi":"10.1016/j.bbamcr.2025.120007","DOIUrl":"10.1016/j.bbamcr.2025.120007","url":null,"abstract":"<div><div>Hypoxia-inducible factors (HIFs) are master regulators of cellular adaptation to hypoxia in both disease and normal physiological conditions. HIFs consist of two subunits: the oxygen-sensitive alpha (α) and the constitutively expressed beta (β). The three oxygen-dependent alpha subunits—HIF-1α, HIF-2α, and HIF-3α—encoded by distinct genes are crucial for regulating cellular responses to hypoxia in various vertebrates, including humans. Much of our understanding of HIFs is based on studies on HIF-1α and HIF-2α subunits. Recent studies have shown that, although HIF-3α is the least studied member, it may also play essential roles in the development of human diseases, including cancer, cardiovascular and respiratory diseases, metabolic disorders, and other pathological processes. In this review, we focus on how HIF-3α overexpression is associated with various human diseases, aiming to better understand its role in human pathophysiology and its potential use as a therapeutic target.</div></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1872 7","pages":"Article 120007"},"PeriodicalIF":4.6,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144271097","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
Delphinidin inhibits the ALOX15-mediated ferroptosis in rats to alleviate myocardial ischemia and reperfusion injury 飞鸽苷抑制alox15介导的大鼠铁下垂,减轻心肌缺血再灌注损伤。
IF 4.6 2区 生物学
Biochimica et biophysica acta. Molecular cell research Pub Date : 2025-06-11 DOI: 10.1016/j.bbamcr.2025.120006
Qing Sun , Mei Lv , Zhen Wang
{"title":"Delphinidin inhibits the ALOX15-mediated ferroptosis in rats to alleviate myocardial ischemia and reperfusion injury","authors":"Qing Sun ,&nbsp;Mei Lv ,&nbsp;Zhen Wang","doi":"10.1016/j.bbamcr.2025.120006","DOIUrl":"10.1016/j.bbamcr.2025.120006","url":null,"abstract":"<div><h3>Objective</h3><div>The present study aimed to investigate the role of delphinidin (Dp) in myocardial ischemia-reperfusion injury (MIRI) and elucidate the underlying mechanism.</div></div><div><h3>Methods</h3><div>MIRI animal models were established in Sprague-Dawley rats by ligation of left anterior descending coronary artery (LAD) ligation for 30 min and reperfusion of 2 h. Primary cardiomyocytes and H9C2 cells were stimulated by oxygen-glucose deprivation/regain (OGD/R) conditions for mimicking MIRI cell models. Ultrasound, hematoxylin and eosin and Masson staining were used to evaluate cardiac function and myocardial infarction in rats following Dp treatment. Cell counting kit-8 assay and flow cytometry were performed to detect cell viability and apoptosis, respectively. Western blotting and quantitative real-time polymerase chain reaction measured ALOX15 expression. Additionally, ferroptosis-related factors and lactate dehydrogenase levels were detected using commercial kits.</div></div><div><h3>Results</h3><div>In MIRI rats, Dp treatment dose-dependently increased the left ventricular ejection fraction (EF) and fractional shortening (FS) while reduced the left ventricular internal diameter in diastole (LVIDd) and systole (LVIDs). The increase of necrosis and fibrosis in cardiac tissues of MIRI rats were relieved by Dp. Dp treatment inhibited the apoptosis and ferroptosis of cardiomyocytes both in vivo and in vitro. Mechanically, Dp docked with a ferroptosis-related protein ALOX15 to induce its degradation. Moreover, ferroptosis activator erastin and ALOX15 overexpression reversed the protective effects of Dp on cardiomyocytes.</div></div><div><h3>Conclusion</h3><div>Dp inhibited ferroptosis by molecular docking ALOX15 and inducing its degradation, thereby improving MIRI.</div></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1872 7","pages":"Article 120006"},"PeriodicalIF":4.6,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144293183","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
Recombinant protein TprK promotes M1 macrophage polarization and phagocytosis by inducing Indoleamine 2,3-dioxygenase protein production 重组蛋白TprK通过诱导吲哚胺2,3-双加氧酶蛋白的产生促进M1巨噬细胞极化和吞噬
IF 4.6 2区 生物学
Biochimica et biophysica acta. Molecular cell research Pub Date : 2025-06-11 DOI: 10.1016/j.bbamcr.2025.120005
Qing-Qi Meng , Ze Li , Zhi-Xuan Huang , Ning-Dai Chen , Wei-Jing Lin , Yue Zhong , Li-Jun Huang , Li-Rong Lin , Xu Shen , Jian-Jun Niu , Tian-Ci Yang
{"title":"Recombinant protein TprK promotes M1 macrophage polarization and phagocytosis by inducing Indoleamine 2,3-dioxygenase protein production","authors":"Qing-Qi Meng ,&nbsp;Ze Li ,&nbsp;Zhi-Xuan Huang ,&nbsp;Ning-Dai Chen ,&nbsp;Wei-Jing Lin ,&nbsp;Yue Zhong ,&nbsp;Li-Jun Huang ,&nbsp;Li-Rong Lin ,&nbsp;Xu Shen ,&nbsp;Jian-Jun Niu ,&nbsp;Tian-Ci Yang","doi":"10.1016/j.bbamcr.2025.120005","DOIUrl":"10.1016/j.bbamcr.2025.120005","url":null,"abstract":"<div><div>Syphilis, caused by <em>Treponema pallidum</em> (<em>T. pallidum</em>), remains a significant global health concern, with its pathogenesis closely linked to immune system interactions. Macrophages play a critical role in host defense, with polarization towards the M1 phenotype contributing to pro-inflammatory responses and pathogen clearance. However, the specific mechanisms through which <em>T. pallidum</em> modulates macrophage activity remain unclear. In this study, we investigated the role of recombinant TprK (rTprK), an outer membrane protein of <em>T. pallidum</em>, in macrophage polarization and phagocytic function. Our findings reveal that rTprK significantly enhances M1 polarization and promotes the production of pro-inflammatory cytokines (<em>P</em> &lt; 0.05). Additionally, we demonstrate that rTprK induces indoleamine 2,3-dioxygenase (IDO) production through the TLR2/JAK1/STAT1 pathway, which is crucial for modulating macrophage function (<em>P</em> &lt; 0.05). Inhibition of TLR2, JAK1, or STAT1 effectively reduces IDO expression and attenuates macrophage activation (<em>P</em> &lt; 0.05). These findings provide novel insights into the immunoregulatory role of rTprK in <em>T. pallidum</em> infection.</div></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1872 7","pages":"Article 120005"},"PeriodicalIF":4.6,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144290996","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
Blocking mutant IDH1 phosphorylation triggers APC/C CDH1-dependent ubiquitination in mitotic cells 阻断突变体IDH1磷酸化触发有丝分裂细胞中APC/C cdh1依赖性泛素化。
IF 4.6 2区 生物学
Biochimica et biophysica acta. Molecular cell research Pub Date : 2025-06-11 DOI: 10.1016/j.bbamcr.2025.120002
Sonam Swain , Nishant Jain
{"title":"Blocking mutant IDH1 phosphorylation triggers APC/C CDH1-dependent ubiquitination in mitotic cells","authors":"Sonam Swain ,&nbsp;Nishant Jain","doi":"10.1016/j.bbamcr.2025.120002","DOIUrl":"10.1016/j.bbamcr.2025.120002","url":null,"abstract":"<div><div>IDH1 mutation occurs early in glioma development; thus, mutant IDH1-specific inhibitors are being developed as glioma therapy. But, recent reports suggest that mutant IDH1 inhibitors treatments result in loss of therapeutic vulnerabilities and makes cells resistant to anticancer agents. To overcome resistance, the new paradigm in drug discovery is to develop molecules that can degrade oncogenes by harnessing cellular ubiquitination machinery. Therefore, it is imperative to identify strategies for degrading mutant IDH1 employing cellular ubiquitination machinery. To address this, we found that concerted action of the mitotic kinases Cdk1/Cyclin B1 and Plk1 increases mutant IDH1 enzyme activity. It is known that phosphorylation is linked to protein stability, phosphorylation of a short linear degron motif or phosphodegron can trigger target protein ubiquitination. By contrast, phosphorylation of constitutively active degron motifs can block target protein ubiquitination - phospho-inactivated degron. As phosphorylation can trigger or block ubiquitination, it is unknown if phosphorylation affects mutant IDH1 ubiquitination in mitosis. Therefore, in this study, we asked if phosphorylation of mutant IDH1 is linked to ubiquitination. To answer this question, we examined ubiquitination of phosphomutants and phosphomimetics of mutant IDH1 in mitosis. We found that blocking IDH1<sup>R132H</sup> phosphorylation is linked to ubiquitination. We observed that APC/C CDH1 ubiquitinates IDH1<sup>R132H-T77A-S94A</sup>. Further, we show that APC/C CDH1 ubiquitinates lysines 301 and 321 in C-terminal domain of IDH1<sup>R132H-T77A-S94A</sup>. Thus, blocking mutant IDH1 phosphorylation triggers APC/C CDH1-dependent ubiquitination in mitotic cells. We suggest employing mitotic inhibitors that also block phosphorylation of mutant IDH1 can ubiquitinate mutant IDH1 in cancer cells.</div></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1872 7","pages":"Article 120002"},"PeriodicalIF":4.6,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144293269","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
Botulinum toxin A prevents hypertrophic scarring by suppressing PARP14/SOCS2-mediated M2 polarization of macrophages 肉毒毒素A通过抑制PARP14/ socs2介导的巨噬细胞M2极化来预防增生性瘢痕形成。
IF 4.6 2区 生物学
Biochimica et biophysica acta. Molecular cell research Pub Date : 2025-06-10 DOI: 10.1016/j.bbamcr.2025.120003
Mohyeddin Ali , Bochao Xie , Pengfei Li , Shuwei Chen , Yao Lu , Fazhi Qi , Ze Xiong , Jianrui Li
{"title":"Botulinum toxin A prevents hypertrophic scarring by suppressing PARP14/SOCS2-mediated M2 polarization of macrophages","authors":"Mohyeddin Ali ,&nbsp;Bochao Xie ,&nbsp;Pengfei Li ,&nbsp;Shuwei Chen ,&nbsp;Yao Lu ,&nbsp;Fazhi Qi ,&nbsp;Ze Xiong ,&nbsp;Jianrui Li","doi":"10.1016/j.bbamcr.2025.120003","DOIUrl":"10.1016/j.bbamcr.2025.120003","url":null,"abstract":"<div><div>Botulinum toxin A (BTXA) is a safe and widely used neurotoxic protein in cosmetic procedures and medical applications. This investigation focuses on the function of BTXA on macrophage phenotype during hypertrophic scar (HS) formation and the underlying functional mechanism. A mouse model of HS was generated, where BTXA treatment reduced dermal thickness, epidermal hyperplasia, and collagen deposition in a dose-dependent manner. Moreover, BTXA reduced fibrosis, proliferation, angiogenesis, and M2 macrophage markers within the scar tissues, with parallel findings obtained in the <em>in vitro</em> co-culture system of induced M2 macrophages (derived from THP-1 monocytes) and human dermal fibroblasts (HDFs). Following bioinformatics and RNA sequencing insights, we identified increased expression of poly (ADP-ribose) polymerase family member 14 (PARP14) and suppressor of cytokine signaling 2 (SOCS2) in wound skin of mice, which were suppressed by BTXA treatment. PARP14 enhanced SOCS2 mRNA stability. Overexpression of PARP14 restored the M2 polarization of macrophages and negated the HS-ameliorating effects of BTXA. However, these effects were counteracted by the additional silencing of SOCS2 in mice or THP-1 cells. In conclusion, this investigation suggests that BTXA inhibits PARP14-mediated SOCS2 RNA stabilization to reduce M2 polarization of macrophages and alleviate hypertrophic scarring.</div></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1872 7","pages":"Article 120003"},"PeriodicalIF":4.6,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144282315","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
Recombinant human ADAMTS13 attenuates LPS-induced acute kidney injury and renal microangiopathy in murine advanced liver fibrosis by cleaving vWF 重组人ADAMTS13通过切割vWF减轻lps诱导的小鼠晚期肝纤维化急性肾损伤和肾微血管病变
IF 4.6 2区 生物学
Biochimica et biophysica acta. Molecular cell research Pub Date : 2025-06-09 DOI: 10.1016/j.bbamcr.2025.120000
Hiroyuki Masuda, Kosuke Kaji, Norihisa Nishimura, Masayoshi Takami, Akihiko Shibamoto, Yuki Tsuji, Koh Kitagawa, Shinya Sato, Hiroaki Takaya, Tadashi Namisaki, Hitoshi Yoshiji
{"title":"Recombinant human ADAMTS13 attenuates LPS-induced acute kidney injury and renal microangiopathy in murine advanced liver fibrosis by cleaving vWF","authors":"Hiroyuki Masuda,&nbsp;Kosuke Kaji,&nbsp;Norihisa Nishimura,&nbsp;Masayoshi Takami,&nbsp;Akihiko Shibamoto,&nbsp;Yuki Tsuji,&nbsp;Koh Kitagawa,&nbsp;Shinya Sato,&nbsp;Hiroaki Takaya,&nbsp;Tadashi Namisaki,&nbsp;Hitoshi Yoshiji","doi":"10.1016/j.bbamcr.2025.120000","DOIUrl":"10.1016/j.bbamcr.2025.120000","url":null,"abstract":"<div><div>Hepatorenal syndrome (HRS) has a poor prognosis among the complication of cirrhosis, yet treatment options are limited. Thrombotic microangiopathy with reduced ADAMTS13 activity and vWF accumulation has been reported to play a key role in the pathogenesis of acute kidney injury (AKI) in cirrhosis. This study investigated the effect of recombinant ADAMTS13 (rADAMTS13) on AKI with carbon tetrachloride (CCl<sub>4</sub>)-induced advanced liver fibrosis in mice. AKI was induced by intraperitoneal administration of acute insult with double dose of CCl<sub>4</sub> and lipopolysaccharide (AKI-F mice), and mice were treated with rADAMTS13 (10 μg/body). AKI-F mice showed a marked liver dysfunction as well as renal dysfunction with elevated serum level of renal damage markers including kidney injury molecule-1, osteopontin, and neutrophil gelatinase-associated lipocalin. In AKI-F mice, reduced plasma ADAMTS13 activity and increased vWF antigen levels resulted in the decrease in hepatic and renal blood flow. Treatment with rADAMTS13 increased plasma ADAMTS13 activity, decreased vWF antigen levels leading to recovery of liver and kidney blood flow. Consequently, both hepatic and renal injuries showed serological and histopathologic improvements with decreased F4/80<sup>+</sup> macrophage infiltration and 4-hydroxynonenal<sup>+</sup> oxidative damage after rADAMTS13 treatment. The deposition of CD41a-positive microthrombi in kidney tissues observed in the AKI-F mice was significantly suppressed by treatment with rADAMTS13. Concomitantly, rADAMTS13 treatment promoted angiogenesis as well as inhibited vascular inflammation in the kidney of AKI-F mice. In conclusion, administration of rADAMTS13 may improve inflammation, oxidative stress, and reduced blood flow in liver and kidney tissues, thereby mitigating hepatorenal syndrome.</div></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1872 7","pages":"Article 120000"},"PeriodicalIF":4.6,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144253978","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
Preface to the Special Issue "Oxidative stress in health and disease". 特刊“健康与疾病中的氧化应激”前言。
IF 4.6 2区 生物学
Biochimica et biophysica acta. Molecular cell research Pub Date : 2025-06-09 DOI: 10.1016/j.bbamcr.2025.119999
Helmut Sies
{"title":"Preface to the Special Issue \"Oxidative stress in health and disease\".","authors":"Helmut Sies","doi":"10.1016/j.bbamcr.2025.119999","DOIUrl":"10.1016/j.bbamcr.2025.119999","url":null,"abstract":"","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":" ","pages":"119999"},"PeriodicalIF":4.6,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144274129","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
USP47 enhances NRP1-mediated angiogenesis to promote gastric cancer progression USP47增强nrp1介导的血管生成促进胃癌进展
IF 4.6 2区 生物学
Biochimica et biophysica acta. Molecular cell research Pub Date : 2025-06-09 DOI: 10.1016/j.bbamcr.2025.120004
Wei Chen , Huizhi Wang , Haitao Sun , Junbo Zuo , Pengcheng Jiang , Wen Feng , Zhenhua Huang
{"title":"USP47 enhances NRP1-mediated angiogenesis to promote gastric cancer progression","authors":"Wei Chen ,&nbsp;Huizhi Wang ,&nbsp;Haitao Sun ,&nbsp;Junbo Zuo ,&nbsp;Pengcheng Jiang ,&nbsp;Wen Feng ,&nbsp;Zhenhua Huang","doi":"10.1016/j.bbamcr.2025.120004","DOIUrl":"10.1016/j.bbamcr.2025.120004","url":null,"abstract":"<div><div>Gastric cancer (GC) is a leading cause of cancer-related mortality, particularly in East Asia, where its incidence remains high. The limited prognosis for advanced GC patients underscores the need for new therapeutic strategies targeting key molecules involved in tumor progression. In this study, we investigated the role of the deubiquitinating enzyme USP47 in GC progression, focusing on its interaction with Neuropilin-1 (NRP1), a co-receptor known to enhance angiogenesis. Our findings reveal that USP47 is significantly overexpressed in GC tissues and correlates with poor patient survival. Through in vitro experiments, we demonstrate that USP47 promotes GC cell proliferation, migration, and invasion. Additionally, USP47 enhances angiogenesis by stabilizing NRP1, preventing its ubiquitination and degradation, and activating the PI3K/Akt signaling pathway. These results suggest that USP47 contributes to GC progression through the regulation of NRP1-mediated angiogenesis, highlighting its potential as a therapeutic target for GC treatment.</div></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1872 7","pages":"Article 120004"},"PeriodicalIF":4.6,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144241428","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
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