International Journal of Biochemistry & Cell Biology最新文献_第3页

Corrigendum to “ROCK inhibition reduces the sensitivity of mutant p53 glioblastoma to genotoxic stress through a Rac1- driven ROS production” [Int. J. Biochem. Mol. Bio. 164 (2023) 106474–106484] “ROCK抑制通过Rac1驱动的ROS产生降低突变型p53胶质母细胞瘤对基因毒性应激的敏感性”的更正[j]。学生物化学j。生物化学学报[j].安徽农业大学学报，2016,34(2):1064 -1064。

IF 3.4 3区生物学

International Journal of Biochemistry & Cell Biology Pub Date : 2025-02-01 DOI: 10.1016/j.biocel.2024.106732

Yuli Thamires Magalhaes, Fabio Luis Forti

引用次数: 0

A testis-specific long non-coding RNA, 1700052I22Rik, regulates spermatid chromatin condensation in mice 睾丸特异性长非编码 RNA 1700052I22Rik 可调节小鼠精子染色质凝聚。

IF 3.4 3区生物学

International Journal of Biochemistry & Cell Biology Pub Date : 2025-02-01 DOI: 10.1016/j.biocel.2024.106725

Mengzhen Li , Zexuan Zhang , Qi Geng , Yan Lu , Shiying Miao , Xingguang Zhang , Wei Song , Kai Li

引用次数: 0

GABPα targeted by miR-378a-5p inhibits the growth and angiogenesis of colorectal carcinoma miR-378a-5p靶向GABPα抑制结直肠癌的生长和血管生成。

IF 3.4 3区生物学

International Journal of Biochemistry & Cell Biology Pub Date : 2025-02-01 DOI: 10.1016/j.biocel.2024.106729

Mengyi Wang , Jiangfa Qi , Zhenlin Tan , Runlong Zhou , Qing Zhuo , Xiaotong Deng , Zhenrong Wang , Ruijie Zhou , Fan Li , Yao Xu

{"title":"GABPα targeted by miR-378a-5p inhibits the growth and angiogenesis of colorectal carcinoma","authors":"Mengyi Wang , Jiangfa Qi , Zhenlin Tan , Runlong Zhou , Qing Zhuo , Xiaotong Deng , Zhenrong Wang , Ruijie Zhou , Fan Li , Yao Xu","doi":"10.1016/j.biocel.2024.106729","DOIUrl":"10.1016/j.biocel.2024.106729","url":null,"abstract":"<div><div>Considering the high degree of malignancy, recurrence rate and poor prognosis, exploring promising targets is an imperious strategy for colorectal carcinoma therapy. Recent studies have indicated that GABPα plays a role in cancer aggressiveness, but its exact function and regulatory mechanisms in colorectal cancer progression remain unclear. This study aims to explore the biological role of GABPα and its upstream regulator, miR-378a-5p, in modulating cancer progression. The expression levels of GABPα and miR-378a-5p were analyzed through comprehensive data mining and qPCR assays. The functional effects of GABPα were assessed using CCK-8, wound healing, transwell invasion assay, tube formation and xenograft model in nude mice. A co-transfection assay was also performed to investigate the regulatory relationship between miR-378a-5p and GABPα. We found that GABPα expression was significantly downregulated in human colorectal cancer tissues and cell lines. Functional assays revealed that GABPα overexpression suppressed the proliferation, migration, invasion and angiogenesis of colorectal cancer cells, and <em>in vivo</em> experiments further confirmed the inhibitory role of GABPα. Additionally, miR-378a-5p was upregulated in colorectal cancer, and GABPα was identified as a direct target of miR-378a-5p, as confirmed by luciferase reporter assays. Furthermore, overexpression of GABPα partially counteracted the enhanced malignant behaviors of cancer cells induced by miR-378a-5p. Our findings suggest that miR-378a-5p promotes the aggressive progression of colorectal cancer by directly targeting GABPα, highlighting this regulatory axis as a potential therapeutic target for colorectal carcinoma.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"179 ","pages":"Article 106729"},"PeriodicalIF":3.4,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142878585","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}

引用次数: 0

Priming human bone marrow-derived mesenchymal stromal cells with signaling modifiers boosts their functionality: Potential application in regenerative therapies 用信号调节剂诱导人骨髓间充质间质细胞增强其功能：在再生治疗中的潜在应用。

IF 3.4 3区生物学

International Journal of Biochemistry & Cell Biology Pub Date : 2025-02-01 DOI: 10.1016/j.biocel.2025.106734

Vaijayanti Kale

{"title":"Priming human bone marrow-derived mesenchymal stromal cells with signaling modifiers boosts their functionality: Potential application in regenerative therapies","authors":"Vaijayanti Kale","doi":"10.1016/j.biocel.2025.106734","DOIUrl":"10.1016/j.biocel.2025.106734","url":null,"abstract":"<div><div>Mesenchymal stromal cells (MSCs) isolated from tissues such as bone marrow, cord, cord blood, etc., are frequently used as feeder layers to expand hematopoietic stem/ progenitor cells (HSCs/HSPCs) in vitro. They are also co-infused with the HSCs to improve the efficacy of transplantation. However, the MSCs sourced from non-hematopoietic tissues could have suboptimal hematopoiesis-supportive ability. Likewise, the functionality of the MSCs is known to decline after continuous in vitro culture – an unavoidable manipulation to get clinically relevant cell numbers. Hence, it may be necessary to boost the hematopoiesis-supportive ability of the long-term cultured MSCs so that they can, in turn, be used to prime the HSCs before their clinical applications. Here, I show that priming human bone marrow-derived MSCs (BMSCs) with appropriately selected signaling modifiers and integrin-activating bioactive peptides boosts their hematopoiesis-supportive ability, as seen by the formation of a significantly higher number of colonies from the bone marrow-derived mononuclear cells (MNCs) and extensive proliferation of CD34<sup>+</sup> HSCS briefly interacted with them. Priming the BMSCs with signaling modifiers is a <em>cost-effective and time-efficient</em> process as synthesizing these small molecule compounds is relatively inexpensive – an advantage in clinical settings. The approach of briefly interacting the donor HSCs/HSPCs with the <em>primed</em> BMSCs just before their infusion into the recipients' bodies could save the cost of long-term ex vivo expansion of HSCs. This concept could also find applications in other regenerative medicine protocols after identifying suitable pharmacological modulators that have the desired effects on the target cells.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"179 ","pages":"Article 106734"},"PeriodicalIF":3.4,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142958254","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}

引用次数: 0

Bemcentinib enhances sensitivity to estrogen receptor inhibitors in breast cancer cells 贝美替尼增强乳腺癌细胞对雌激素受体抑制剂的敏感性

IF 3.4 3区生物学

International Journal of Biochemistry & Cell Biology Pub Date : 2025-02-01 DOI: 10.1016/j.biocel.2025.106750

Gyeongmi Kim , Se Hee Ahn , Se-Kyeong Jang , Selim Kim , Hyunggee Kim , Ki Soo Park , Hyeon-Ok Jin , Chan Sub Park , Min-Ki Seong , Hyun-Ah Kim , In-Chul Park

{"title":"Bemcentinib enhances sensitivity to estrogen receptor inhibitors in breast cancer cells","authors":"Gyeongmi Kim , Se Hee Ahn , Se-Kyeong Jang , Selim Kim , Hyunggee Kim , Ki Soo Park , Hyeon-Ok Jin , Chan Sub Park , Min-Ki Seong , Hyun-Ah Kim , In-Chul Park","doi":"10.1016/j.biocel.2025.106750","DOIUrl":"10.1016/j.biocel.2025.106750","url":null,"abstract":"<div><div>Estrogen receptor (ER)-positive breast cancer accounts for a substantial proportion of breast cancer cases and is typically managed using ER inhibitors, such as tamoxifen and fulvestrant. However, the development of resistance to these therapies is a significant clinical challenge, and the improvement of therapeutic strategies is crucial. This study aimed to investigate the potential of bemcentinib, a well-known AXL inhibitor, to enhance the sensitivity of MCF7 breast cancer cells to 4-hydroxytamoxifen (4-OHT) and fulvestrant. Our findings revealed that bemcentinib effectively decreased S6K1 phosphorylation and synergistically induced cell death when used in combination with ER inhibitors. Bemcentinib treatment also unexpectedly activated STAT3, and inhibition of STAT3 enhanced cell death induced by bemcentinib and 4-OHT. Notably, the combination of bemcentinib and 4-OHT effectively induced cell death even in tamoxifen-resistant MCF7 cells (MCF7-TR), highlighting its potential to overcome tamoxifen resistance. Interestingly, AXL knockdown did not enhance the sensitivity to 4-OHT or affect S6K1 signaling in either MCF7 or MCF7-TR cells, suggesting that the sensitizing effect of bemcentinib through S6K1 inhibition may be independent of AXL expression. Our findings suggest that bemcentinib treatment, particularly in combination therapy, could be a promising strategy for improving treatment efficacy and overcoming tamoxifen resistance in ER-positive breast cancer.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"180 ","pages":"Article 106750"},"PeriodicalIF":3.4,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143124082","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}

引用次数: 0

Ethacrynic acid inhibits the growth and proliferation of prostate cancer cells by targeting GSTP1 and regulating the PI3K-AKT signaling pathway 乙丙酸通过靶向GSTP1，调控PI3K-AKT信号通路抑制前列腺癌细胞的生长和增殖。

IF 3.4 3区生物学

International Journal of Biochemistry & Cell Biology Pub Date : 2025-02-01 DOI: 10.1016/j.biocel.2025.106740

Bin Zhao , Bingfeng Zhang , Minhao Chenzhang , Kangxian Jiang , Dianyu Wang , Junyi Chen

{"title":"Ethacrynic acid inhibits the growth and proliferation of prostate cancer cells by targeting GSTP1 and regulating the PI3K-AKT signaling pathway","authors":"Bin Zhao , Bingfeng Zhang , Minhao Chenzhang , Kangxian Jiang , Dianyu Wang , Junyi Chen","doi":"10.1016/j.biocel.2025.106740","DOIUrl":"10.1016/j.biocel.2025.106740","url":null,"abstract":"<div><h3>Background</h3><div>As a diuretic, ethacrynic acid (EA) has been shown to play a suppressive role in cancers, including prostate cancer (PC). However, its molecular regulatory mechanism is still unclear. Therefore, our study is centered on investigating the effect of EA on PC development and its mechanism.</div></div><div><h3>Methods</h3><div>To verify the binding relationship between EA and GSTP1, molecular docking and cellular thermal shift assay (CETSA) were conducted. To examine how EA affects PC cell proliferation, cell cycle, and apoptosis, cell function assays were performed. qRT-PCR was used to detect GSTP1 mRNA expression. The expression of GSTP1 protein and PI3K-AKT signaling pathway-related proteins in cells was detected by western blot (WB). To verify how EA and GSTP1 influence cell growth in PC, <em>in vivo</em> experiments were conducted.</div></div><div><h3>Results</h3><div>The binding relationship between GSTP1 and EA was confirmed by molecular docking and CETSA results. Cell experiments showed that EA could hinder PI3K/AKT pathway and PC cell proliferation, arrest the cell cycle in G0/G1 phase, and facilitate apoptosis by binding to GSTP1. <em>In vivo</em> experiments in nude mice verified that the interaction between EA and GSTP1 reduced PI3K and AKT phosphorylation and inhibited the growth of PC cells.</div></div><div><h3>Conclusion</h3><div>EA inhibits PC progression by binding to GSTP1 to downregulate the activity of PI3K/AKT pathway, and this result suggests the potential of EA to be an anticancer agent for PC therapy.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"180 ","pages":"Article 106740"},"PeriodicalIF":3.4,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143124095","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}

引用次数: 0

Transcription factors, nucleotide excision repair, and cancer: A review of molecular interplay 转录因子、核苷酸切除修复与癌症：分子相互作用综述》。

IF 3.4 3区生物学

International Journal of Biochemistry & Cell Biology Pub Date : 2025-02-01 DOI: 10.1016/j.biocel.2024.106724

Perihan Yagmur Guneri-Sozeri, Ogün Adebali

{"title":"Transcription factors, nucleotide excision repair, and cancer: A review of molecular interplay","authors":"Perihan Yagmur Guneri-Sozeri, Ogün Adebali","doi":"10.1016/j.biocel.2024.106724","DOIUrl":"10.1016/j.biocel.2024.106724","url":null,"abstract":"<div><div>Bulky DNA adducts are mostly formed by external factors such as UV irradiation, smoking or treatment with DNA crosslinking agents. If such DNA adducts are not removed by nucleotide excision repair, they can lead to formation of driver mutations that contribute to cancer formation. Transcription factors (TFs) may critically affect both DNA adduct formation and repair efficiency at the binding site to DNA. For example, \"hotspot\" mutations in melanoma coincide with UV-induced accumulated cyclobutane pyrimidine dimer (CPD) adducts and/or inhibited repair at the binding sites of some TFs. Similarly, anticancer treatment with DNA cross-linkers may additionally generate DNA adducts leading to secondary mutations and the formation of malignant subclones. In addition, some TFs are overexpressed in response to UV irradiation or chemotherapeutic treatment, activating oncogenic and anti-oncogenic pathways independently of nucleotide excision repair itself. This review focuses on the interplay between TFs and nucleotide excision repair during cancer development and progression.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"179 ","pages":"Article 106724"},"PeriodicalIF":3.4,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142822895","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}

引用次数: 0

Prevention of fenitrothion induced hepatic toxicity by saponarin via modulating TLR4/MYD88, JAK1/STAT3 and NF-κB signaling pathways 皂苷通过调控TLR4/MYD88、JAK1/STAT3和NF-κB信号通路预防菲诺硫磷诱导的肝毒性

IF 3.4 3区生物学

International Journal of Biochemistry & Cell Biology Pub Date : 2025-02-01 DOI: 10.1016/j.biocel.2024.106716

Hesham M. Hassan , Mahmoud El Safadi , Muhammad Faisal Hayat , Ahmed Al-Emam

{"title":"Prevention of fenitrothion induced hepatic toxicity by saponarin via modulating TLR4/MYD88, JAK1/STAT3 and NF-κB signaling pathways","authors":"Hesham M. Hassan , Mahmoud El Safadi , Muhammad Faisal Hayat , Ahmed Al-Emam","doi":"10.1016/j.biocel.2024.106716","DOIUrl":"10.1016/j.biocel.2024.106716","url":null,"abstract":"<div><div>Fenitrothion (FEN) is an organophosphate insecticidal agent that is considered as major source of organs toxicity. Saponarin (SAP) is a naturally occurring novel flavone that exhibits a wide range of medicinal properties. The current trial was conducted to evaluate the ameliorative potential of SAP against FEN instigated liver toxicity in rats. Thirty-two male albino rats were apportioned into four groups including control, FEN (10 mg/kg), FEN (10 mg/kg) + SAP (80 mg/kg), and SAP (80 mg/kg) alone treated group. It was revealed that FEN administration upregulated the gene expression of TNF-α, TLR4, IL-1β, MYD88, IL-6, TRAF6, COX-2, NF-κB, JAK1 and STAT3 while reducing the gene expression of IκB. Moreover, the levels of reactive oxygen species (ROS) and malondialdehyde (MDA) were increased while the activities of catalase (CAT), glutathione peroxidase (GPx), superoxide dismutase (SOD), heme-oxygenase-1 (HO-1) and glutathione reductase (GSR) were decreased after FEN exposure. Furthermore, FEN administration notably escalated the levels of hepatic enzymes including alanine transaminase (ALT), aspartate aminotransferase (AST), gamma-glutamyl transferase (GGT) and alkaline phosphatase (ALP) whereas reduced the levels of total proteins and albumin. Besides, FEN intake upregulated the levels of Caspase-9, Bax and Caspase-3 while reducing the levels of Bcl-2. Hepatic histology was impaired after FEN intoxication. Nonetheless, SAP treatment remarkably protected the normal state of liver via regulating abovementioned irregularities. Our <em>in-silico</em> analysis confirmed that SAP hold that potential to interact with binding pocket of these proteins, highlighting its ability as a therapeutic compound to alleviate FEN-induced liver damage.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"179 ","pages":"Article 106716"},"PeriodicalIF":3.4,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142792454","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}

引用次数: 0

Disulfiram/copper induces BAK-mediated caspase-independent apoptosis in MCF-7 cells 双硫仑/铜诱导bac介导的MCF-7细胞非caspase依赖性凋亡。

IF 3.4 3区生物学

International Journal of Biochemistry & Cell Biology Pub Date : 2025-02-01 DOI: 10.1016/j.biocel.2024.106731

Beini Sun , Yu Wang , Hongce Chen , Qialing Huang , Chunchun An , Qiuqiang Zhan , Xiaoping Wang , Tongsheng Chen

{"title":"Disulfiram/copper induces BAK-mediated caspase-independent apoptosis in MCF-7 cells","authors":"Beini Sun , Yu Wang , Hongce Chen , Qialing Huang , Chunchun An , Qiuqiang Zhan , Xiaoping Wang , Tongsheng Chen","doi":"10.1016/j.biocel.2024.106731","DOIUrl":"10.1016/j.biocel.2024.106731","url":null,"abstract":"<div><div>Disulfiram (DSF) and copper (Cu<sup>2 +</sup>) in combination exhibit powerful anti-cancer effect on a variety of cancer cell lines. Here, we found that DSF/Cu<sup>2+</sup> facilitated the accumulation of intracellular reactive oxygen species (ROS), and induced ROS-dependent apoptosis accompanied by chromatin condensation and phosphatidylserine externalization in MCF-7 cells. DSF/Cu<sup>2+</sup> caused caspase-independent apoptosis by promoting the AIF translocation from mitochondria to nucleus. Most importantly, the cytotoxicity of DSF/Cu<sup>2+</sup> was markedly inhibited by knocking out AIF, suggesting the indispensability of AIF in DSF/Cu<sup>2+</sup>-induced apoptosis. The pro-apoptotic protein BAK instead of BAX was upregulated and activated upon DSF/Cu<sup>2+</sup> treatment, and the <em>BAK</em> knockout cells exhibited high resistance to DSF/Cu<sup>2+</sup>, indicating the importance of BAK in DSF/Cu<sup>2+</sup>-induced apoptosis. Additionally, both co-immunoprecipitation and live-cell quantitative fluorescence resonance energy transfer (FRET) analysis revealed that DSF/Cu<sup>2+</sup> unlocked the binding of MCL-1 to BAK, which resulted in subsequent BAK homo-oligomerization. Overall, our data demonstrate for the first time that DSF/Cu<sup>2+</sup> unlocks the binding of MCL-1 to BAK, thus leading BAK oligomerization and subsequent AIF nucleus translocation to mediate caspase-independent apoptosis in MCF-7 cells.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"179 ","pages":"Article 106731"},"PeriodicalIF":3.4,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142886399","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}

引用次数: 0

SENP2 as a critical regulator in liver ischemia-reperfusion injury SENP2是肝脏缺血再灌注损伤的关键调节因子。

IF 3.4 3区生物学

International Journal of Biochemistry & Cell Biology Pub Date : 2025-01-29 DOI: 10.1016/j.biocel.2025.106741

Lei Zheng , Shuling Han , Olivia M Martinez , Sheri M Krams

{"title":"SENP2 as a critical regulator in liver ischemia-reperfusion injury","authors":"Lei Zheng , Shuling Han , Olivia M Martinez , Sheri M Krams","doi":"10.1016/j.biocel.2025.106741","DOIUrl":"10.1016/j.biocel.2025.106741","url":null,"abstract":"<div><h3>Background and Aims</h3><div>Liver ischemia-reperfusion injury (LIRI) profoundly affects liver function and survival largely through activation of the innate immune system. In this study we sought to elucidate the underlying mechanisms by which the innate immune system impacts liver function and survival in LIRI.</div></div><div><h3>Approach and Results</h3><div>RNA-seq analyses, from existing datasets of liver from mice with LIRI, was performed to identify differentially expressed genes (DEGs) associated with LIRI. Protein-protein interaction analysis revealed clusters involved in signaling pathways with a cluster anchored by Senp2, acting as a central modulator. Macrophages and monocytes were determined to be the source of Senp2 with monocyte-derived macrophages expressing the highest levels of Senp2. Experiments in a mouse model of LIRI further elucidated the expression, function, and mechanism of Senp2. Overexpression of Senp2 suppressed both the polarization of M1 macrophages and the production of inflammatory mediators. Further, Senp2-overexpressing macrophages significantly ameliorated LIRI.</div></div><div><h3>Conclusions</h3><div>Our study suggests that SENP2 plays an important role in regulating LIRI by influencing macrophage polarization through the Dvl2/GSK-3β/β-catenin axis. While further validation is needed, these findings indicate that targeting SENP2-mediated pathways could be a promising approach for mitigating LIRI and enhancing therapeutic strategies.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"180 ","pages":"Article 106741"},"PeriodicalIF":3.4,"publicationDate":"2025-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143076204","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}

引用次数: 0