International Journal of Biochemistry & Cell Biology最新文献_第10页

MEST promotes immune escape in gastric cancer by downregulating MHCI expression via SHP2 MEST 通过 SHP2 下调 MHCI 的表达，促进胃癌的免疫逃逸

IF 3.4 3区生物学

International Journal of Biochemistry & Cell Biology Pub Date : 2024-08-22 DOI: 10.1016/j.biocel.2024.106621

Min Huang , Fan Zhang , Yan Zhu, Hai Zeng, Shuang Li

{"title":"MEST promotes immune escape in gastric cancer by downregulating MHCI expression via SHP2","authors":"Min Huang , Fan Zhang , Yan Zhu, Hai Zeng, Shuang Li","doi":"10.1016/j.biocel.2024.106621","DOIUrl":"10.1016/j.biocel.2024.106621","url":null,"abstract":"<div><h3>Background</h3><p>Immune escape is a major obstacle to T-cell-based immunotherapy for cancers such as gastric cancer (GC). Mesoderm-specific transcript (MEST) is a tumor-promoting factor that regulates multiple oncogenic signaling pathways. However, the role of MEST-mediated immune escape is unclear.</p></div><div><h3>Methods</h3><p>Bioinformatics analysis of MEST expression and enrichment pathways were performed Quantitative reverse transcription PCR (qPCR) or western blot was used to detect the expression of MEST, Src homology region 2-containing protein tyrosine phosphatase 2 (SHP2), Major histocompatibility class I (MHCI)-related genes. Cell function was assessed by Cell Counting Kit (CCK)-8, Transwell, Lactate dehydrogenase (LDH) kit, flow cytometry, enzyme-linked immunosorbent assay (ELISA), and immunohistochemistry (IHC). Xenograft nude mice and immune-reconstructed mice were used to test the effects of different treatments on tumor growth and immune escape <em>in vivo</em>.</p></div><div><h3>Results</h3><p>MEST was upregulated in GC and promoted tumor proliferation, migration, and invasion. Rescue experiments revealed that TNO155 treatment or knockdown of SHP2 promoted the killing ability of CD8<sup>+</sup> T cells and the expression of granzyme B (GZMB) and interferon-gamma (IFN-γ), and MEST overexpression reversed the effect. <em>In vivo</em> experiments confirmed that MEST promoted tumor growth, knockdown of MEST inhibited immune escape in GC, and that combination treatment with anti-PD-1 improved anti-tumor activity.</p></div><div><h3>Conclusion</h3><p>In this study, we demonstrated that MEST inhibited IFN-γ secretion from CD8+ T cells by up-regulating SHP2, thereby downregulating MHCI expression in GC cells to promote immune escape and providing a new T cell-based therapeutic potential for GC.</p></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"174 ","pages":"Article 106621"},"PeriodicalIF":3.4,"publicationDate":"2024-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142044307","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

ITCH inhibits alkaliptosis in human pancreatic cancer cells through YAP1-dependent SLC16A1 activation ITCH 通过 YAP1 依赖性 SLC16A1 激活抑制人类胰腺癌细胞的碱中毒。

IF 3.4 3区生物学

International Journal of Biochemistry & Cell Biology Pub Date : 2024-08-22 DOI: 10.1016/j.biocel.2024.106646

Xiutao Cai , Fangquan Chen , Hu Tang , Dandan Chao , Rui Kang , Daolin Tang , Jiao Liu

{"title":"ITCH inhibits alkaliptosis in human pancreatic cancer cells through YAP1-dependent SLC16A1 activation","authors":"Xiutao Cai , Fangquan Chen , Hu Tang , Dandan Chao , Rui Kang , Daolin Tang , Jiao Liu","doi":"10.1016/j.biocel.2024.106646","DOIUrl":"10.1016/j.biocel.2024.106646","url":null,"abstract":"<div><p>Alkaliptosis is a type of pH-dependent cell death and plays an emerging role in tumor suppression. However, the key modulation mechanism of alkaliptosis remains largely unknown. In particular, the nucleus, as the centre of genetic and metabolic regulation, is crucial for the regulation of cellular life. It is not known whether nuclear proteins are involved in the regulation of alkaliptosis. Here, we isolated nuclear proteins to perform a proteomics that identified itchy E3 ubiquitin protein ligase (ITCH) as a natural inhibitor of alkaliptosis in human pancreatic ductal adenocarcinoma (PDAC) cells. The downregulation of ITCH protein is associated with the induction of alkaliptosis in three human PDAC cell lines (SW1990, MiaPaCa2, and PANC1). Functionally, increasing ITCH expression reduces JTC801-induced growth inhibition and cell death. In contrast, knocking down <em>ITCH</em> using specific shRNA increases JTC801-induced cell growth inhibition in the short or long term, resulting in increased cell death. Mechanistically, JTC801-induced ITCH inhibition blocks large tumor suppressor kinase 1 (LATS1) ubiquitination, which in turn suppresses Yes1 associated transcriptional regulator (YAP1)-dependent the transcriptional activation of solute carrier family 16 member 1 (SLC16A1), a proton-linked monocarboxylate transporter that inhibits JTC801-induced alkaliptosis. Additionally, decreased expression of <em>ITCH</em> is associated with longer survival times in patients with PDAC. Collectively, our results establish an ITCH-dependent pathway that regulates alkaliptotic sensitivity in PDAC cells and deepen the understanding of alkaliptosis in targeted therapy.</p></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"175 ","pages":"Article 106646"},"PeriodicalIF":3.4,"publicationDate":"2024-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142047400","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

IRX3 promotes adipose tissue browning and inhibits fibrosis in obesity-resistant mice IRX3 可促进肥胖小鼠脂肪组织棕色化并抑制纤维化。

IF 3.4 3区生物学

International Journal of Biochemistry & Cell Biology Pub Date : 2024-08-22 DOI: 10.1016/j.biocel.2024.106638

Xi-yue Yan , Yuan-yuan Luo , Hui-jian Chen , Xiao-qin Hu , Peng Zheng , Hong-ting Fang , Fei Ding , Li Zhang , Zhen Li , You-e Yan

{"title":"IRX3 promotes adipose tissue browning and inhibits fibrosis in obesity-resistant mice","authors":"Xi-yue Yan , Yuan-yuan Luo , Hui-jian Chen , Xiao-qin Hu , Peng Zheng , Hong-ting Fang , Fei Ding , Li Zhang , Zhen Li , You-e Yan","doi":"10.1016/j.biocel.2024.106638","DOIUrl":"10.1016/j.biocel.2024.106638","url":null,"abstract":"<div><p>Obesity is one of the threats to human health and survival. High fat diet (HFD)-induced obesity leads to adipose tissue fibrosis and a series of metabolic diseases. There are some people still thin under HFD, a phenomenon known as the \"obesity resistance (OR) phenotype\". It was found that Iroquois homeobox 3 (<em>IRX3</em>) is considered as a regulator in obesity, but the regulatory mechanism between OR and <em>IRX3</em> is still unclear. In this study, we investigated OR on a HFD and the role of the <em>IRX3</em> gene. Using mice, we observed that OR mice had lower body weights, reduced liver lipid synthesis, and increased white adipose tissue (WAT) lipolysis compared to obesity-prone (OP) mice. Additionally, OR mice exhibited spontaneous WAT browning and less fibrosis, correlating with higher <em>Irx3</em> expression. Utilizing 3T3-L1 differentiated adipocytes, our study demonstrated that overexpression of <em>Irx3</em> promoted thermogenesis-related gene expression and reduced adipocyte fibrosis. Therefore, <em>Irx3</em> promotes WAT browning and inhibits fibrosis in OR mice. These results provide insight into the differences between obesity and OR, new perspectives on obesity treatment, and guidance for lessening adipose tissue fibrosis.</p></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"175 ","pages":"Article 106638"},"PeriodicalIF":3.4,"publicationDate":"2024-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142037597","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

Tumor-derived exosomal ICAM1 promotes bone metastasis of triple-negative breast cancer by inducing CD8+ T cell exhaustion 肿瘤外源性 ICAM1 通过诱导 CD8+ T 细胞衰竭促进三阴性乳腺癌的骨转移。

IF 3.4 3区生物学

International Journal of Biochemistry & Cell Biology Pub Date : 2024-08-13 DOI: 10.1016/j.biocel.2024.106637

Mingcang Chen , Zhengwei Fu , Chunyu Wu

{"title":"Tumor-derived exosomal ICAM1 promotes bone metastasis of triple-negative breast cancer by inducing CD8+ T cell exhaustion","authors":"Mingcang Chen , Zhengwei Fu , Chunyu Wu","doi":"10.1016/j.biocel.2024.106637","DOIUrl":"10.1016/j.biocel.2024.106637","url":null,"abstract":"<div><p>Exosomes, which are nanosized extracellular vesicles, have emerged as crucial mediators of the crosstalk between tumor cells and the immune system. Intercellular adhesion molecule 1 (ICAM1) plays a crucial role in multiple immune functions as well as in the occurrence, development and metastasis of cancer. As a glycoprotein expressed on the cell membrane, ICAM1 is secreted extracellularly on exosomes and regulates the immunosuppressive microenvironment. However, the role of exosomal ICAM1 in the immune microenvironment of breast cancer bone metastases remains unclear. This study aimed to elucidated the role of exosomal ICAM1 in facilitating CD8+ T cell exhaustion and subsequent bone metastasis in triple-negative breast cancer (TNBC). We demonstrated that TNBC cells release ICAM1-enriched exosomes, and the binding of ICAM1 to its receptor is necessary for the suppressive effect of CD8 T cell proliferation and function. This pivotal engagement not only inhibits CD8+ T cell proliferation and activation but also initiates the development of an immunosuppressive microenvironment that is conducive to TNBC tumor growth and bone metastasis. Moreover, ICAM1 blockade significantly impairs the ability of tumor exosomes to bind to CD8+ T cells, thereby inhibiting their immunosuppressive effects. The present study elucidates the complex interaction between primary tumors and the immune system that is mediated by exosomes and provides a foundation for the development of novel cancer immunotherapies that target ICAM1 with the aim of mitigating TNBC bone metastasis.</p></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"175 ","pages":"Article 106637"},"PeriodicalIF":3.4,"publicationDate":"2024-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141989367","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

ACAP3 negatively regulated by HDAC2 inhibits the malignant development of papillary thyroid carcinoma cells 受 HDAC2 负调控的 ACAP3 可抑制甲状腺乳头状癌细胞的恶性发展。

IF 3.4 3区生物学

International Journal of Biochemistry & Cell Biology Pub Date : 2024-08-03 DOI: 10.1016/j.biocel.2024.106635

Fenfen Zhan , Ronghui Zhang , Lanlan Qiu , Yuezhong Ren

{"title":"ACAP3 negatively regulated by HDAC2 inhibits the malignant development of papillary thyroid carcinoma cells","authors":"Fenfen Zhan , Ronghui Zhang , Lanlan Qiu , Yuezhong Ren","doi":"10.1016/j.biocel.2024.106635","DOIUrl":"10.1016/j.biocel.2024.106635","url":null,"abstract":"<div><p>ArfGAP with coiled-coil, ankyrin repeat and PH domains 3 (ACAP3) level has been confirmed to be downregulated in papillary thyroid carcinoma (PTC). Histone deacetylase inhibitors (HDACIs) have therapeutic effects on PTC. Accordingly, this study probed into the potential relation of histone deacetylase 2 (HDAC2) and ACAP3 in PTC. Expressions of ACAP3 and HDAC2 in PTC were investigated by quantitative real-time polymerase chain reaction (qRT-PCR). The relationship between HDAC2 and ACAP3 was predicted by Pearson analysis. Cell functional assays (cell counting kit-8, transwell, wound healing and flow cytometry assays) and rescue assay were carried out to determine the effects of HDAC2/ACAP3 axis on biological behaviors of PTC cells. Expressions of apoptosis-, epithelial-mesenchymal transition-, Protein Kinase B (AKT)-, and P53-related proteins were measured by Western blot. ACAP3 level was downregulated in PTC tissues and cells. ACAP3 overexpression (oe-ACAP3) suppressed viability, proliferation, migration and invasion of PTC cells, facilitated apoptosis, downregulated the expressions of Protein Kinase B (Bcl-2) and N-cadherin, upregulated the expressions of Bcl-2 associated protein X (Bax) and E-cadherin, diminished the p-AKT/AKT ratio and elevated the p-p53/p53 ratio; however, ACAP3 silencing or HDAC2 overexpression (oe-HDAC2) did the opposite. HDAC2 negatively correlated with ACAP3. The tumor-suppressing effect of oe-ACAP3 in PTC was reversed by oe-HDAC2. Collectively, ACAP3 negatively regulated by HDAC2 suppresses the proliferation and metastasis while facilitating apoptosis of PTC cells.</p></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"174 ","pages":"Article 106635"},"PeriodicalIF":3.4,"publicationDate":"2024-08-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141890702","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

RNA-based logic for selective protein expression in senescent cells 基于 RNA 的衰老细胞蛋白质选择性表达逻辑。

IF 3.4 3区生物学

International Journal of Biochemistry & Cell Biology Pub Date : 2024-07-31 DOI: 10.1016/j.biocel.2024.106636

Ward Jacobs , Masoomeh Khalifeh , Merijn Koot , Valentina Palacio-Castañeda , Jenny van Oostrum , Marleen Ansems , Wouter P.R. Verdurmen , Roland Brock

{"title":"RNA-based logic for selective protein expression in senescent cells","authors":"Ward Jacobs , Masoomeh Khalifeh , Merijn Koot , Valentina Palacio-Castañeda , Jenny van Oostrum , Marleen Ansems , Wouter P.R. Verdurmen , Roland Brock","doi":"10.1016/j.biocel.2024.106636","DOIUrl":"10.1016/j.biocel.2024.106636","url":null,"abstract":"<div><p>Cellular senescence is a cellular state characterized by irreversible growth arrest, resistance to apoptosis and secretion of inflammatory molecules, which is causally linked to the pathogenesis of many age-related diseases. Besides, there is accumulating evidence that selective removal of senescent cells can benefit therapies for cancer and fibrosis by modulating the inflammatory microenvironment. While the field of so-called senolytics has spawned promising small molecules and peptides for the selective removal of senescent cells, there is still no effective means to detect senescent cells <em>in vivo</em>, a prerequisite for understanding the role of senescence in pathophysiology and to assess the effectiveness of treatments aimed at removing senescent cells. Here, we present a strategy based on an mRNA logic circuit, that yields mRNA-dependent protein expression only when a senescence-specific miRNA signature is present. Following a validation of radiation-induced senescence induction in primary human fibroblasts, we identify miRNAs up- and downregulated in association with cellular senescence using RT-qPCR. Incorporating binding sites to these miRNAs into the 3’ untranslated regions of the mRNA logic circuit, we demonstrate the senescence-specific expression of EGFP for detection of senescent cells and of a constitutively active caspase-3 for selective removal. Altogether, our results pave the way for a novel approach to execute an mRNA-based programme specifically in senescent cells aimed at their detection or selective removal.</p></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"174 ","pages":"Article 106636"},"PeriodicalIF":3.4,"publicationDate":"2024-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1357272524001286/pdfft?md5=127b2de5e49efd58380aad8dcd997168&pid=1-s2.0-S1357272524001286-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141876560","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}

引用次数: 0

The role of nicotinic acetylcholine receptors in the pathophysiology and pharmacotherapy of autism spectrum disorder: Focus on α7 nicotinic receptors 烟碱乙酰胆碱受体在自闭症谱系障碍的病理生理学和药物治疗中的作用：聚焦α7烟碱受体。

IF 3.4 3区生物学

International Journal of Biochemistry & Cell Biology Pub Date : 2024-07-31 DOI: 10.1016/j.biocel.2024.106634

Murat Oz , Lina Al Kury , Bassem Sadek , Mohamed Omer Mahgoub

{"title":"The role of nicotinic acetylcholine receptors in the pathophysiology and pharmacotherapy of autism spectrum disorder: Focus on α7 nicotinic receptors","authors":"Murat Oz , Lina Al Kury , Bassem Sadek , Mohamed Omer Mahgoub","doi":"10.1016/j.biocel.2024.106634","DOIUrl":"10.1016/j.biocel.2024.106634","url":null,"abstract":"<div><p>Postmortem studies have revealed that brains of individuals with autism spectrum disorder (ASD) exhibit abnormalities in various components of the cholinergic system including cholinergic receptors, projections, and nuclei. Deletions in the 15q13.3 region which encompasses <em>CHRNA7,</em> the gene that encodes the α7-nACh receptor, have been linked to various neurodevelopmental disorders, including ASD. In addition, the involvement of α7-nACh receptors in biological phenomena known to play a role in the pathophysiology of ASD such as cognitive functions, learning, memory, neuroinflammation, and oxidative stress, as well as the excitation-inhibition balance in neuronal circuits and maternal immune activation have been reported in previous studies. Furthermore, evolving preclinical and clinical literature supports the potential therapeutic benefits of using selectively acting cholinergic compounds, particularly those targeting the α7-nACh receptor subtype, in the treatment of ASD. This study reviews the previous literature on the involvement of nACh receptors in the pathophysiology of ASD and focuses on the α7-nACh receptor as a potential therapeutic target.</p></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"174 ","pages":"Article 106634"},"PeriodicalIF":3.4,"publicationDate":"2024-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141879698","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

Corrigendum to “Graphene oxide leads to mitochondrial-dependent apoptosis by activating ROS-p53-mPTP pathway in intestinal cells” [Int. J. Biochem. Cell Biol. 146 (2022) 106206] 更正："氧化石墨烯通过激活肠道细胞中的 ROS-p53-mPTP 通路导致线粒体依赖性凋亡" [Int. J. Biochem. Cell Biol. 146 (2022) 106206]。

IF 3.4 3区生物学

International Journal of Biochemistry & Cell Biology Pub Date : 2024-07-25 DOI: 10.1016/j.biocel.2024.106633

Weiyu Feng, Jinbang Wang, Baodong Li, Yonggang Liu, Dongli Xu, Ke Cheng, Jing Zhuang

引用次数: 0

Iron metabolism in doxorubicin-induced cardiotoxicity: From mechanisms to therapies 多柔比星诱发心脏毒性的铁代谢：从机制到疗法。

IF 3.4 3区生物学

International Journal of Biochemistry & Cell Biology Pub Date : 2024-07-23 DOI: 10.1016/j.biocel.2024.106632

Hua Ye , Lin Wu , Yanmei Liu

引用次数: 0

NS8593 inhibits chondrocyte ferroptosis and alleviates cartilage injury in rat adjuvant arthritis through TRPM7 / HO-1 pathway NS8593通过TRPM7/HO-1途径抑制大鼠佐剂性关节炎软骨细胞的铁突变并减轻软骨损伤。

IF 3.4 3区生物学

International Journal of Biochemistry & Cell Biology Pub Date : 2024-07-23 DOI: 10.1016/j.biocel.2024.106618

Wenjuan Hao , Rendi Zhu , Hailin Zhang , Yong Chen , Shufang Li , Fuli Zhou , Wei Hu , Renpeng Zhou

{"title":"NS8593 inhibits chondrocyte ferroptosis and alleviates cartilage injury in rat adjuvant arthritis through TRPM7 / HO-1 pathway","authors":"Wenjuan Hao , Rendi Zhu , Hailin Zhang , Yong Chen , Shufang Li , Fuli Zhou , Wei Hu , Renpeng Zhou","doi":"10.1016/j.biocel.2024.106618","DOIUrl":"10.1016/j.biocel.2024.106618","url":null,"abstract":"<div><p>Ferroptosis is an emerging target in rheumatoid arthritis (RA). We previously reported that transient receptor potential melastatin 7 (TRPM7) expression is correlated with RA cartilage destruction and demonstrated that TRPM7 mediates ferroptosis in chondrocytes. Here, we further determined the role and mechanism of (R)-N-(Benzimidazol-2-yl)-1,2,3,4-tetrahydro-1-naphthylamine (NS8593), a TRPM7 inhibitor, in chondrocyte ferroptosis of RA. We established <em>in vitro</em> models of ferroptosis in human chondrocytes (C28/I2 cells) by using ferroptosis inducer Erastin. The results showed that NS8593 could protect C28/I2 cells from ferroptosis by inhibiting TRPM7 channel, which was manifested by restoring cell viability, reducing cytotoxicity, affecting the expression of ferroptosis marker protein, and restoring redox balance to alleviate Erastin-induced oxidative stress injury. Mechanistically, the Heme oxygenase-1 (HO-1) axis responded to Erastin stimulation, which resulted in TRPM7-mediated chondrocyte ferroptosis, NS8593 could reduce the expression of HO-1 by inhibiting TRPM7 channel. Moreover, NS8593 alleviated articular cartilage destruction and inhibited chondrocyte ferroptosis in AA rats. In conclusion, NS8593 mitigated articular cartilage damage and chondrocyte ferroptosis through the TRPM7/HO-1 pathway, suggesting that NS8593 may be a potential novel drug for the treatment of RA.</p></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"174 ","pages":"Article 106618"},"PeriodicalIF":3.4,"publicationDate":"2024-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141762324","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