Cellular signalling最新文献

Expression of concern: The emerging crosstalk between atherosclerosis-related microRNAs and Bermuda triangle of foam cells: Cholesterol influx, trafficking, and efflux. 表达关切：动脉粥样硬化相关 microRNA 与泡沫细胞百慕大三角之间新出现的串扰：胆固醇流入、贩运和外流。

IF 4.4 2区生物学

Cellular signalling Pub Date : 2024-12-01 Epub Date: 2024-09-07 DOI: 10.1016/j.cellsig.2024.111394

引用次数: 0

Sestrin2 balances mitophagy and apoptosis through the PINK1-Parkin pathway to attenuate severe acute pancreatitis. Sestrin2通过PINK1-Parkin途径平衡有丝分裂和细胞凋亡，从而减轻重症急性胰腺炎。

IF 4.4 2区生物学

Cellular signalling Pub Date : 2024-11-20 DOI: 10.1016/j.cellsig.2024.111518

Yuxi Yang, Yiqiu Peng, Yingying Li, Tingjuan Shi, Ning Xu, Yingyi Luan, Chenghong Yin

{"title":"Sestrin2 balances mitophagy and apoptosis through the PINK1-Parkin pathway to attenuate severe acute pancreatitis.","authors":"Yuxi Yang, Yiqiu Peng, Yingying Li, Tingjuan Shi, Ning Xu, Yingyi Luan, Chenghong Yin","doi":"10.1016/j.cellsig.2024.111518","DOIUrl":"https://doi.org/10.1016/j.cellsig.2024.111518","url":null,"abstract":"<p><p>Mitophagy serves as a mitochondrial quality control mechanism to maintain the homeostasis of mitochondria and the intracellular environment. Studies have shown that there is a close relationship between mitophagy and apoptosis. Sestrin2 (Sesn2) is a highly conserved class of stress-inducible proteins that play important roles in reducing oxidative stress damage, inflammation, and apoptosis. However, the potential mechanism of how Sesn2 regulates mitophagy and apoptosis in severe acute pancreatitis (SAP) remains unclear. In the study, RAW264.7 (macrophage cell Line) cellular inflammation model established by lipopolysaccharide (LPS) treatment as well as LPS and CAE-induced SAP mouse model (wild-type and Sen2 Knockout mouse) were used. Our study showed that LPS stimulation significantly increased the level of Sesn2 in RAW264.7 cells, Sesn2 increased mitochondrial membrane potential, decreased inflammation levels, mitochondrial superoxide levels and apoptosis, and also promoted monocyte macrophages toward the M2 anti-inflammatory phenotype, suggesting a protective effect of Sesn2 on mitochondria. Further, Sesn2 increased mitophagy and decreased apoptosis via modulating the PINK1-Parkin signaling. Meanwhile, knockout of Sesn2 exacerbated pancreatic, mitochondrial damage and inflammation in a mouse model of SAP. In addition, the protective effect of Sesn2 against SAP was shown to be associated with mitophagy conducted by the PINK1-Parkin pathway via inhibiting apoptosis. These findings reveal that Sesn2 in balancing mitochondrial autophagy and apoptosis by modulating the PINK1-Parkin signaling may present a new therapeutic strategy for the treatment of SAP.</p>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":" ","pages":"111518"},"PeriodicalIF":4.4,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142692373","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

TSG101 overexpression enhances metastasis in oral squamous cell carcinoma through cell cycle regulation. TSG101 过表达可通过细胞周期调控增强口腔鳞状细胞癌的转移。

IF 4.4 2区生物学

Cellular signalling Pub Date : 2024-11-19 DOI: 10.1016/j.cellsig.2024.111519

Yang Yang, Xiao-Le Wang, Ye-Xin Yue, Gang Chen, Hou-Fu Xia

{"title":"TSG101 overexpression enhances metastasis in oral squamous cell carcinoma through cell cycle regulation.","authors":"Yang Yang, Xiao-Le Wang, Ye-Xin Yue, Gang Chen, Hou-Fu Xia","doi":"10.1016/j.cellsig.2024.111519","DOIUrl":"https://doi.org/10.1016/j.cellsig.2024.111519","url":null,"abstract":"<p><p>The tumor susceptibility gene 101 (TSG101) was firstly identified as a tumor-inhibiting factor in 1996. Subsequent studies gradually revealed its crucial role in several important cellular processes, including cell survival, vesicle transportation, viral infection, etc. Additionally, TSG101 has been identified as an oncoprotein in certain tumorigenic processes. These conflicting findings suggest that TSG101 might exhibit tumor heterogeneity. Currently, the expression pattern and function of TSG101 in oral squamous cell carcinoma (OSCC) are still untouched. Herein, we reported that TSG101 expression is upregulated and is associated with poorer survival and a higher propensity for lymph node metastasis in OSCC patients. In vivo mouse models confirmed that TSG101 down-regulation effectively inhibited the pulmonary metastases of human OSCC cells. In vitro cell experiments not only proved that TSG101 knockdown significantly disrupted metastasis-related phenotypes in different OSCC cell lines, but also revealed that TSG101 possibly controls the cell cycle through regulating the transcription of Cyclin A/B to play these roles. Additionally, we further validated these findings with a mouse cell line and murine orthotopic OSCC models. Collectively, the oncoprotein function of TSG101 in OSCC is evident from this study. We offer fresh insights into the heterogeneity of TSG101 and highlight new potential targets for OSCC management.</p>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":" ","pages":"111519"},"PeriodicalIF":4.4,"publicationDate":"2024-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142686154","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

TXN promotes tumorigenesis by activating the ERK1/2 and ERK5 signaling pathways regulating c-Myc in non-small cell lung cancer. TXN 通过激活调节非小细胞肺癌 c-Myc 的 ERK1/2 和 ERK5 信号通路来促进肿瘤发生。

IF 4.4 2区生物学

Cellular signalling Pub Date : 2024-11-19 DOI: 10.1016/j.cellsig.2024.111517

Xiaoting Liu, Xilin Dong, YiFan Hu, Cong Dong, Sanzhu Wu, Yanan Fang, Yaxin Hu

{"title":"TXN promotes tumorigenesis by activating the ERK1/2 and ERK5 signaling pathways regulating c-Myc in non-small cell lung cancer.","authors":"Xiaoting Liu, Xilin Dong, YiFan Hu, Cong Dong, Sanzhu Wu, Yanan Fang, Yaxin Hu","doi":"10.1016/j.cellsig.2024.111517","DOIUrl":"https://doi.org/10.1016/j.cellsig.2024.111517","url":null,"abstract":"<p><p>Lung cancer is the primary cause of cancer-related deaths worldwide, particularly for non-small cell lung cancer (NSCLC). However, the exact mechanism underlying tumor formation remains unclear. It is widely acknowledged that inflammation and oxidative stress occur in the tumor microenvironment, promoting cell malignant growth and metastasis. Thioredoxin-1 (TXN), the main regulator of oxidative stress, plays a significant role in the development of NSCLC. However, the specific tumor-promoting mechanism is still being investigated. This study aimed to examine the function and mechanism of TXN in NSCLC. The effects of knockdown or overexpression TXN on cell proliferation, invasion and apoptosis were evaluated by Cell Counting Kit-8, colony formation, wound healing, transwell, TUNEL staining, and flow cytometric assays. Western blotting was performed to analyze the regulation of TXN and downstream proteins suppressed by genes and pharmacology. TXN knockdown significantly suppressed cell proliferation, invasion and promoted apoptosis both in vitro and in vivo, whereas TXN overexpression reversed these malignant phenotypes. We found that TXN regulated c-Myc expression through ERK1/2 and ERK5 signaling pathways. Suppressing ERK1/2 led to the compensatory activation of ERK5, and simultaneously inhibiting ERK1/2 and ERK5 synergistically reduced c-Myc expression, further attenuating cell proliferation, invasion and enhanced apoptosis. Our results indicated tumor promotion of TXN in NSCLC and TXN regulated c-Myc in the interest of tumorigenesis through ERK1/2 and ERK5 signaling pathways. Targeting TXN and blocking the ERK1/2 and ERK5 pathways could potentially offer new therapeutic strategies for NSCLC.</p>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":" ","pages":"111517"},"PeriodicalIF":4.4,"publicationDate":"2024-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142686158","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

PacBio full-length transcriptome analysis reveals the role of tRNA-like structures in RNA processing. PacBio 全长转录组分析揭示了 tRNA 样结构在 RNA 处理中的作用。

IF 4.4 2区生物学

Cellular signalling Pub Date : 2024-11-19 DOI: 10.1016/j.cellsig.2024.111515

Yanping Hu, Shuangyong Yan, Haohao Yan, Jingping Su, Zhongqiu Cui, Junling Li, Shengjun Wang, Yue Sun, Wenjing Li, Shan Gao

{"title":"PacBio full-length transcriptome analysis reveals the role of tRNA-like structures in RNA processing.","authors":"Yanping Hu, Shuangyong Yan, Haohao Yan, Jingping Su, Zhongqiu Cui, Junling Li, Shengjun Wang, Yue Sun, Wenjing Li, Shan Gao","doi":"10.1016/j.cellsig.2024.111515","DOIUrl":"https://doi.org/10.1016/j.cellsig.2024.111515","url":null,"abstract":"<p><strong>Background: </strong>Mitochondrial DNA (mtDNA) and chloroplast DNA (cpDNA) are distinct from nuclear DNA (nuDNA) in a eukaryotic cell. Animal mitochondria transcribe a single primary transcript that carries all genes from a DNA strand; In contrast, plant mitochondria and chloroplasts produce multiple primary transcripts, with each transcript carrying several genes. How primary transcripts of plant mtDNA and cpDNA are processed into mature RNAs is still unknown.</p><p><strong>Results: </strong>In the present study, we employed PacBio's full-length transcriptome data to characterize the transcription of Arabidopsis thaliana mtDNA, providing a more comprehensive and precise understanding. The primary findings included 20 novel mitochondrial (mt) RNAs of A. thaliana, transcripts carrying single introns or exons, long mt and chloroplast (cp) tRNAs with intricate secondary structures, and the role of tRNA-like structures in RNA processing. The gene of No. 20 novel mt RNA and its paralog on chromosome 2 of A. thaliana were assigned locus IDs ATMG01335 and AT2G07811.</p><p><strong>Conclusions: </strong>According to our upgraded \"mitochondrial cleavage\" model, tRNA-like structures serve as \"punctuation\" marks for RNA processing, akin to the role of tRNAs. Both tRNA-like structures and tRNAs collaborate for RNA processing in plant mitochondria and chloroplasts.</p>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":" ","pages":"111515"},"PeriodicalIF":4.4,"publicationDate":"2024-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142686087","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

C1GALT1 high expression enhances the progression of glioblastoma through the EGFR-AKT/ERK cascade. C1GALT1的高表达会通过表皮生长因子受体-AKT/ERK级联反应促进胶质母细胞瘤的进展。

IF 4.4 2区生物学

Cellular signalling Pub Date : 2024-11-17 DOI: 10.1016/j.cellsig.2024.111513

Yanting Su, Xin Ao, Yunfeng Long, Zhengrong Zhang, Mingzhu Zhang, Zhenwang Zhang, Mingjie Wei, Shigang Shan, Surui Lu, You Yu, Bo Xu

{"title":"C1GALT1 high expression enhances the progression of glioblastoma through the EGFR-AKT/ERK cascade.","authors":"Yanting Su, Xin Ao, Yunfeng Long, Zhengrong Zhang, Mingzhu Zhang, Zhenwang Zhang, Mingjie Wei, Shigang Shan, Surui Lu, You Yu, Bo Xu","doi":"10.1016/j.cellsig.2024.111513","DOIUrl":"10.1016/j.cellsig.2024.111513","url":null,"abstract":"<p><p>Core1 β1,3-galactosyltransferase (C1GALT1) is an essential glycotransferase controlling the elongation of GalNAc-type O-glycosylation and its altered expression contributes tumor progression in various cancers. However, the mechanism how C1GALT1 influences gliomas remains unclear. Here，our results from The Cancer Genome Atlas (TCGA) database, The Chinese Glioma Genome Atlas (CGGA) database and the Clinical Proteomic Tumor Analysis Consortium (CPTAC) database showed that the expression of C1GALT1 was increased in higher grade gliomas namely glioblastoma compared with low grade gliomas or non-tumor tissues and significantly associated with poor survival. Downregulation of C1GALT1 suppressed cell proliferation, invasion, and migration in glioma cell lines. Consistent with the result in vitro, C1GALT1 knockdown distinctly inhibited the weight and tumor growth in nude mice. Mechanistically, C1GALT1 knockdown decreased the level of terminal galactose O-glycosylation and phosphorylation on epidermal growth factor receptor (EGFR). Moreover, The AKT/ERK phosphorylation was attenuated in C1GALT1 knockdown cells. And C1GALT1 knockdown decreased the expression of cyclinD1, matrix metalloproteinase 9 (MMP9) through the AKT/ERK signaling pathway Furthermore, transcription factor SP1 which the expression was found to be associated the C1GALT1 expression could bind to the promoter of C1GALT1 gene and regulated its expression. In conclusion, our data show that C1GALT1 enhances the progression of glioma by regulated the O-glycosylation and phosphorylation of EGFR and the subsequent downstream AKT/ERK signaling pathway. Therefore, C1GALT1 represents a potential target for the diagnosis and treatment of glioma.</p>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":" ","pages":"111513"},"PeriodicalIF":4.4,"publicationDate":"2024-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142675096","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

Vericiguat enhances the therapeutic efficacy of mesenchymal stem cells-derived exosomes in acute myocardial infarction through microRNA-1180-3p/ETS1 pathway. 韦立克通过microRNA-1180-3p/ETS1途径增强间充质干细胞外泌体对急性心肌梗死的疗效

IF 4.4 2区生物学

Cellular signalling Pub Date : 2024-11-16 DOI: 10.1016/j.cellsig.2024.111512

Chunyu Li, Chongming Zheng, Yanan Pu, Haoyang Zhou, Ying Li, Weiwei Wang, Xufeng Chen, Cheng Zhang, Yan Chen

{"title":"Vericiguat enhances the therapeutic efficacy of mesenchymal stem cells-derived exosomes in acute myocardial infarction through microRNA-1180-3p/ETS1 pathway.","authors":"Chunyu Li, Chongming Zheng, Yanan Pu, Haoyang Zhou, Ying Li, Weiwei Wang, Xufeng Chen, Cheng Zhang, Yan Chen","doi":"10.1016/j.cellsig.2024.111512","DOIUrl":"10.1016/j.cellsig.2024.111512","url":null,"abstract":"<p><p>Reversing cardiac fibrosis contributes to the restoration of cardiac function in acute myocardial infarction (MI). Exosomes-derived mesenchymal stem cells (MSCs) have been established as potential biomarkers of cardiovascular diseases. While vericiguat has demonstrated promising outcomes in MI via reverse hypertrophy and fibrosis, previous studies about vericiguat pretreatment with MSCs is limited. We aim at exploring whether exosomes derived from vericiguat pretreatment MSCs could augment cardioprotective function and the underlying mechanisms. In our study, exosomes isolated from MSCs (MSC-Exo) and pretreated with vericiguat (MSC<sup>VER</sup>-Exo) were administered to cardiac fibroblasts (CFs) in vitro and male infarcted Sprague-Dawley rat hearts in vivo. In vivo, MSC<sup>VER</sup>-Exo could significantly improve cardiac function and attenuate cardiac fibrosis and decrease the expression of α-smooth muscle actin (α-SMA), Ι and III collagen (Col Ι and Col III) compared to MSC-Exo treatment. In vitro, MSC<sup>VER</sup>-Exo could also restrain proliferation, migration, and the profibrotic genes expression in CFs. miR-1180-3p was enrich in MSC<sup>VER</sup>-Exo. Besides, miR-1180-3p could be delivered to CFs via Exo and alleviated TGF-β1-induced fibrosis through inhibiting ETS1 signaling. The elucidation of this mechanism suggested that exosomes derived from vericiguat pretreatment MSCs could improve cardioprotective effects through promoting CFs function. MiR-1180-3p targeting ETS1 played an important role in antifibrosis.</p>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":" ","pages":"111512"},"PeriodicalIF":4.4,"publicationDate":"2024-11-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142647005","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

Regulation and functions of the DLC family of RhoGAP proteins: Implications for development and cancer RhoGAP 蛋白 DLC 家族的调控和功能：对发育和癌症的影响。

IF 4.4 2区生物学

Cellular signalling Pub Date : 2024-11-15 DOI: 10.1016/j.cellsig.2024.111505

Yannick Frey , Cristiana Lungu , Monilola A. Olayioye

{"title":"Regulation and functions of the DLC family of RhoGAP proteins: Implications for development and cancer","authors":"Yannick Frey , Cristiana Lungu , Monilola A. Olayioye","doi":"10.1016/j.cellsig.2024.111505","DOIUrl":"10.1016/j.cellsig.2024.111505","url":null,"abstract":"<div><div>The DLC (Deleted in Liver Cancer) family of RhoGAP (Rho GTPase-activating) proteins has been extensively studied since the identification of the first family member nearly 30 years ago. Rho GTPase signaling is essential for various cellular processes, including cytoskeletal dynamics, cell migration, and proliferation. Members of the DLC family are key regulators of this signaling pathway, with well-established roles in development and carcinogenesis. Here, we provide a comprehensive review of research into DLC regulation and cellular functions over the last three decades. In particular, we summarize control mechanisms of DLC gene expression at both the transcriptional and post-transcriptional level. Additionally, recent advances in understanding the post-translational regulation of DLC proteins that allow for tuning of protein activity and localization are highlighted. This detailed overview will serve as resource for future studies aimed at further elucidating the complex regulatory mechanisms of DLC family proteins and exploring their potential as targets for therapeutic applications.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"125 ","pages":"Article 111505"},"PeriodicalIF":4.4,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142643868","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

IRAK2 overexpression restrains prostate cancer progression by regulation of TRAF6 ubiquitination IRAK2 过表达可通过调节 TRAF6 泛素化抑制前列腺癌的进展。

IF 4.4 2区生物学

Cellular signalling Pub Date : 2024-11-15 DOI: 10.1016/j.cellsig.2024.111508

Yunfeng Shi, Chengshuai Wu, Chengyue Wang, Ying Shen, Anqi Jiang, Kai Cao, Xiaowu Liu, Xinying Jiang, Zhong Lv

{"title":"IRAK2 overexpression restrains prostate cancer progression by regulation of TRAF6 ubiquitination","authors":"Yunfeng Shi, Chengshuai Wu, Chengyue Wang, Ying Shen, Anqi Jiang, Kai Cao, Xiaowu Liu, Xinying Jiang, Zhong Lv","doi":"10.1016/j.cellsig.2024.111508","DOIUrl":"10.1016/j.cellsig.2024.111508","url":null,"abstract":"<div><div>Prostate cancer is recognized as one of the most common tumors among men worldwide, yet the molecular mechanisms underlying its progression remain to be fully understood. In this study, we explored the role of interleukin-1 receptor-associated kinase 2 (IRAK2) in the progression of prostate cancer. We discovered that IRAK2 expression is downregulated in prostate cancer tissues and cells. Functional assays, including MTT, transwell assays, wound healing assays, and in vivo xenograft models, demonstrated that upregulation of IRAK2 significantly inhibited prostate cancer cell viability, migration, invasion, and tumor growth. Furthermore, we found that IRAK2 modulates the biological functions of prostate cancer by interacting with TNF receptor-associated factor 6 (TRAF6). Knockdown of TRAF6 reversed the suppressive effects of IRAK2 overexpression on prostate cancer cell progression. Additionally, IRAK2 was found to suppress the ubiquitination and degradation of TRAF6 in prostate cancer cells. IRAK2 also influenced the sensitivity of prostate cancer cells to docetaxel (DTX), and silencing IRAK2 reversed the anti-tumor effects of DTX on prostate cancer cells. Our findings suggest that IRAK2 functions as a tumor suppressor in prostate cancer and may serve as a potential therapeutic target for developing effective treatments for prostate cancer.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"125 ","pages":"Article 111508"},"PeriodicalIF":4.4,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142643866","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 synergistic protective effects of paeoniflorin and β-ecdysterone against cardiac hypertrophy through suppressing oxidative stress and ferroptosis. 芍药苷和 β-蜕皮激素通过抑制氧化应激和铁变态对心脏肥大具有协同保护作用

IF 4.4 2区生物学

Cellular signalling Pub Date : 2024-11-15 DOI: 10.1016/j.cellsig.2024.111509

Peimei Yan, Xue Li, Yuhui He, Yanyan Zhang, Yingwanqi Wang, Jianing Liu, Shan Ren, Dingxiao Wu, Yu Zhao, Lin Ding, Weiwei Jia, Ying Lyu, Dan Xiao, Song Lin, Yan Lin

{"title":"The synergistic protective effects of paeoniflorin and β-ecdysterone against cardiac hypertrophy through suppressing oxidative stress and ferroptosis.","authors":"Peimei Yan, Xue Li, Yuhui He, Yanyan Zhang, Yingwanqi Wang, Jianing Liu, Shan Ren, Dingxiao Wu, Yu Zhao, Lin Ding, Weiwei Jia, Ying Lyu, Dan Xiao, Song Lin, Yan Lin","doi":"10.1016/j.cellsig.2024.111509","DOIUrl":"10.1016/j.cellsig.2024.111509","url":null,"abstract":"<p><p>Exploring feasible drugs for the treatment of pathological cardiac hypertrophy has always been a focus of cardiovascular disease research. Paeoniflorin (PF) and β-Ecdysterone (β-Ecd) are the main active components of Paeonia lactiflora and Achyranthes bidentata, which can be used for the treatment of cardiovascular diseases, but their mechanism of action remains unclear. This study focused on oxidative stress and ferroptosis to investigate the protective effects of PF and β-Ecd on cardiac hypertrophy in primary cardiomyocytes and C57BL/6 mice, utilizing the integration of CCK8 assays, ROS detection, molecular docking, real-time quantitative PCR, western blot, immunofluorescence, etc. The result of combination indices demonstrated a significant synergistic protective effect of PF and β-Ecd on cardiac hypertrophy. Furthermore, in vitro and in vivo studies further showed that the combination of PF and β-Ecd could improve the abnormalities of cell surface area, ANP, β-MHC, MDA, SOD, calcium ion, mitochondrial membrane potential and so on induced by cardiac hypertrophy through the inhibition effects of oxidative stress and iron metabolism, which might be closely related to the impact on the Nrf2/HO-1 and SLC7A11/GPX4 pathways. Altogether, this work revealed the mechanism of the combination of PF and β-Ecd in the treatment of cardiac hypertrophy from the aspects of suppressing oxidative stress and ferroptosis, aiming to promote effective treatment of the disease and the clinical application of PF and β-Ecd.</p>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":" ","pages":"111509"},"PeriodicalIF":4.4,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142643869","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