Cunxin Zhang, Qian Wang, Kang Li, Maoqing Fu, Kai Gao, Chao-liang Lv
{"title":"Rosuvastatin: A Potential Therapeutic Agent for Inhibition of Mechanical Pressure-Induced Intervertebral Disc Degeneration","authors":"Cunxin Zhang, Qian Wang, Kang Li, Maoqing Fu, Kai Gao, Chao-liang Lv","doi":"10.2147/jir.s461348","DOIUrl":"https://doi.org/10.2147/jir.s461348","url":null,"abstract":"","PeriodicalId":506013,"journal":{"name":"Journal of Inflammation Research","volume":"21 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141397473","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Yinan Cao, Fan Li, Zhenxuan Sun, Jin Liu, Jie Liu, Qi Yang, Peng Ge, Yalan Luo, Hailong Chen
Purpose: Explore the therapeutic effects and regulatory mechanism of Qingyi Decoction (QYD) on severe acute pancreatitis (SAP) associated acute lung injury (ALI). Methods: We identified the constituents absorbed into the blood of QYD based on a network pharmacological strategy. The differentially expressed genes from the GEO database were screened to identify the critical targets of QYD treatment of SAP-ALI. The SAP-ALI rat model was constructed.Some methods were used to evaluate the efficacy and mechanism of QYD in treating SAP-ALI. LPS-stimulated pulmonary microvascular endothelial cell injury simulated the SAP-induced pulmonary endothelial injury model. We further observed the therapeutic effect of QYD and CDK5 plasmid transfection on endothelial cell injury. Results: 18 constituents were absorbed into the blood, and 764 targets were identified from QYD, 25 of which were considered core targets for treating SAP-ALI. CDK5 was identified as the most critical gene. The results of differential expression analysis showed that the mRNA expression level of CDK5 in the blood of SAP patients was significantly up-regulated compared with that of healthy people. Animal experiments have demonstrated that QYD can alleviate pancreatic and lung injury inflammatory response and reduce the upregulation of CDK5 in lung tissue. QYD or CDK5 inhibitors could decrease the expression of NFAT5 and GEF-H1, and increase the expression of ACE-tub in SAP rat lung tissue. Cell experiments proved that QYD could inhibit the expression of TNF-α and IL-6 induced by LPS. Immunofluorescence results suggested that QYD could alleviate the cytoskeleton damage of endothelial cells, and the mechanism might be related to the inhibition of CDK5-mediated activation of NFAT5, GEF-H1, and ACE-tub. Conclusion: CDK5 has been identified as a critical target for pulmonary endothelial injury of SAP-ALI. QYD may partially alleviate microtubule disassembly by targeting the CDK5/NFAT5/GEF-H1 signaling pathway, thus relieving SAP-induced pulmonary micro-vascular endothelial cell injury.
{"title":"Regulation of Microtubule Stability in Pulmonary Microvascular Endothelial Cells in Rats with Severe Acute Pancreatitis: Qingyi Decoction is a Potential CDK5 Inhibitor","authors":"Yinan Cao, Fan Li, Zhenxuan Sun, Jin Liu, Jie Liu, Qi Yang, Peng Ge, Yalan Luo, Hailong Chen","doi":"10.2147/jir.s451755","DOIUrl":"https://doi.org/10.2147/jir.s451755","url":null,"abstract":"Purpose: Explore the therapeutic effects and regulatory mechanism of Qingyi Decoction (QYD) on severe acute pancreatitis (SAP) associated acute lung injury (ALI). Methods: We identified the constituents absorbed into the blood of QYD based on a network pharmacological strategy. The differentially expressed genes from the GEO database were screened to identify the critical targets of QYD treatment of SAP-ALI. The SAP-ALI rat model was constructed.Some methods were used to evaluate the efficacy and mechanism of QYD in treating SAP-ALI. LPS-stimulated pulmonary microvascular endothelial cell injury simulated the SAP-induced pulmonary endothelial injury model. We further observed the therapeutic effect of QYD and CDK5 plasmid transfection on endothelial cell injury. Results: 18 constituents were absorbed into the blood, and 764 targets were identified from QYD, 25 of which were considered core targets for treating SAP-ALI. CDK5 was identified as the most critical gene. The results of differential expression analysis showed that the mRNA expression level of CDK5 in the blood of SAP patients was significantly up-regulated compared with that of healthy people. Animal experiments have demonstrated that QYD can alleviate pancreatic and lung injury inflammatory response and reduce the upregulation of CDK5 in lung tissue. QYD or CDK5 inhibitors could decrease the expression of NFAT5 and GEF-H1, and increase the expression of ACE-tub in SAP rat lung tissue. Cell experiments proved that QYD could inhibit the expression of TNF-α and IL-6 induced by LPS. Immunofluorescence results suggested that QYD could alleviate the cytoskeleton damage of endothelial cells, and the mechanism might be related to the inhibition of CDK5-mediated activation of NFAT5, GEF-H1, and ACE-tub. Conclusion: CDK5 has been identified as a critical target for pulmonary endothelial injury of SAP-ALI. QYD may partially alleviate microtubule disassembly by targeting the CDK5/NFAT5/GEF-H1 signaling pathway, thus relieving SAP-induced pulmonary micro-vascular endothelial cell injury.","PeriodicalId":506013,"journal":{"name":"Journal of Inflammation Research","volume":"54 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140778290","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Zhen-Zhen Wang, Hang Li, Anish Maskey, K. Srivastava, Changda Liu, Nan Yang, Taoyun Xie, Ziyi Fu, Junxiong Li, Xiaohong Liu, Hugh Sampson, Xiu-Min Li
{"title":"The Efficacy & Molecular Mechanisms of a Terpenoid Compound Ganoderic Acid C1 on Corticosteroid-Resistant Neutrophilic Airway Inflammation: In vivo and in vitro Validation","authors":"Zhen-Zhen Wang, Hang Li, Anish Maskey, K. Srivastava, Changda Liu, Nan Yang, Taoyun Xie, Ziyi Fu, Junxiong Li, Xiaohong Liu, Hugh Sampson, Xiu-Min Li","doi":"10.2147/jir.s433430","DOIUrl":"https://doi.org/10.2147/jir.s433430","url":null,"abstract":"","PeriodicalId":506013,"journal":{"name":"Journal of Inflammation Research","volume":"27 3","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140771795","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background: Tuberculosis (TB) is one of the most infectious diseases caused by Mycobacterium tuberculosis ( M. tb ), and the diagnosis of active tuberculosis (TB) and latent TB infection (LTBI) remains challenging
{"title":"Construction of Immune-Related Diagnostic Model for Latent Tuberculosis Infection and Active Tuberculosis","authors":"Zhihua Zhang, Yuhong Wang, Yankun Zhang, Shujun Geng, Haifeng Wu, Yanxin Shao, Guannan Kang","doi":"10.2147/jir.s451338","DOIUrl":"https://doi.org/10.2147/jir.s451338","url":null,"abstract":"Background: Tuberculosis (TB) is one of the most infectious diseases caused by Mycobacterium tuberculosis ( M. tb ), and the diagnosis of active tuberculosis (TB) and latent TB infection (LTBI) remains challenging","PeriodicalId":506013,"journal":{"name":"Journal of Inflammation Research","volume":"110 ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140785513","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Siyang Cao, Yihao Wei, Yaohang Yue, Ao Xiong, Hui Zeng
: During the past decade, mounting evidence has increasingly linked programmed cell death (PCD) to the progression and development of osteoarthritis (OA). There is a significant need for a thorough scientometric analysis that recapitulates the relationship between PCD and OA. This study aimed to collect articles and reviews focusing on PCD in OA, extracting data from January 1st, 2013, to October 31st, 2023, using the Web of Science. Various tools, including VOSviewer, CiteSpace, Pajek, Scimago Graphica, and the R package, were employed for scientometric and visualization analyses. Notably, China, the USA, and South Korea emerged as major contributors, collectively responsible for more than 85% of published papers and significantly influencing research in this field. Among different institutions, Shanghai Jiao Tong University, Xi’an Jiao Tong University, and Zhejiang University exhibited the highest productivity. Prolific authors included Wang Wei, Wang Jing, and Zhang Li. Osteoarthritis and Cartilage had the most publications in this area. Keywords related to PCD in OA prominently highlighted ‘chondrocytes’, ‘inflammation’, and ‘oxidative stress’, recognized as pivotal mechanisms contributing to PCD within OA. This study presents the first comprehensive scientometric analysis, offering a broad perspective on the knowledge framework and evolving patterns concerning PCD in relation to OA over the last decade. Such insights can aid researchers in comprehensively understanding this field and provide valuable directions for future explorations.
:在过去十年中，越来越多的证据表明程序性细胞死亡（PCD）与骨关节炎（OA）的进展和发展有关。目前亟需对PCD与OA之间的关系进行全面的科学计量分析。本研究旨在通过科学网（Web of Science）收集2013年1月1日至2023年10月31日期间有关OA中PCD的文章和综述。研究使用了多种工具，包括VOSviewer、CiteSpace、Pajek、Scimago Graphica和R软件包，进行科学计量学和可视化分析。值得注意的是，中国、美国和韩国是论文的主要贡献者，共发表了 85% 以上的论文，对该领域的研究产生了重大影响。在不同院校中，上海交通大学、西安交通大学和浙江大学的论文产量最高。多产作者包括王伟、王静和张莉。骨关节炎与软骨》是该领域发表论文最多的期刊。与OA中的PCD相关的关键词主要集中在 "软骨细胞"、"炎症 "和 "氧化应激"，它们被认为是导致OA中PCD的关键机制。本研究首次进行了全面的科学计量学分析，从广阔的视角探讨了过去十年中与 OA 相关的 PCD 知识框架和演变模式。这些见解有助于研究人员全面了解这一领域，并为未来的探索提供有价值的方向。
{"title":"Zooming in and Out of Programmed Cell Death in Osteoarthritis: A Scientometric and Visualized Analysis","authors":"Siyang Cao, Yihao Wei, Yaohang Yue, Ao Xiong, Hui Zeng","doi":"10.2147/jir.s462722","DOIUrl":"https://doi.org/10.2147/jir.s462722","url":null,"abstract":": During the past decade, mounting evidence has increasingly linked programmed cell death (PCD) to the progression and development of osteoarthritis (OA). There is a significant need for a thorough scientometric analysis that recapitulates the relationship between PCD and OA. This study aimed to collect articles and reviews focusing on PCD in OA, extracting data from January 1st, 2013, to October 31st, 2023, using the Web of Science. Various tools, including VOSviewer, CiteSpace, Pajek, Scimago Graphica, and the R package, were employed for scientometric and visualization analyses. Notably, China, the USA, and South Korea emerged as major contributors, collectively responsible for more than 85% of published papers and significantly influencing research in this field. Among different institutions, Shanghai Jiao Tong University, Xi’an Jiao Tong University, and Zhejiang University exhibited the highest productivity. Prolific authors included Wang Wei, Wang Jing, and Zhang Li. Osteoarthritis and Cartilage had the most publications in this area. Keywords related to PCD in OA prominently highlighted ‘chondrocytes’, ‘inflammation’, and ‘oxidative stress’, recognized as pivotal mechanisms contributing to PCD within OA. This study presents the first comprehensive scientometric analysis, offering a broad perspective on the knowledge framework and evolving patterns concerning PCD in relation to OA over the last decade. Such insights can aid researchers in comprehensively understanding this field and provide valuable directions for future explorations.","PeriodicalId":506013,"journal":{"name":"Journal of Inflammation Research","volume":"226 ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140760085","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
: Ferroptosis, a type of programmed cell death that relies on iron, is distinct in terms of its morphological, biochemical and genetic features. Unlike other forms of cell death, such as autophagy, apoptosis, necrosis
{"title":"Unraveling the Molecular Regulation of Ferroptosis in Respiratory Diseases","authors":"Lujian Zhu, Jing Zhou, Chen Yu, Lei Gu, Qin Wang, Hanglu Xu, Yin Zhu, Maodong Guo, Minli Hu, Wei Peng, Hao Fang, Haizhen Wang","doi":"10.2147/jir.s457092","DOIUrl":"https://doi.org/10.2147/jir.s457092","url":null,"abstract":": Ferroptosis, a type of programmed cell death that relies on iron, is distinct in terms of its morphological, biochemical and genetic features. Unlike other forms of cell death, such as autophagy, apoptosis, necrosis","PeriodicalId":506013,"journal":{"name":"Journal of Inflammation Research","volume":"642 ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140757768","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
京公网安备 11010802042870号
京ICP备2023020795号-1
扫码关注我们
求助内容：
应助结果提醒方式：