Journal of pharmaceutical analysis最新文献

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A promising strategy of brain targeted delivery for the treatment of Parkinson's disease: Cyclodextrin supramolecular inclusion complex based thermosensitive gel. 一种治疗帕金森病的有前途的脑靶向递送策略:环糊精超分子包合复合物热敏凝胶。
Journal of pharmaceutical analysis Pub Date : 2025-05-01 Epub Date: 2024-09-13 DOI: 10.1016/j.jpha.2024.101102
Yan-Qiu Wang, Li-Ming Wang, Li-Feng Han, Yi-Bing Chen, Yuan-Lu Cui
{"title":"A promising strategy of brain targeted delivery for the treatment of Parkinson's disease: Cyclodextrin supramolecular inclusion complex based thermosensitive gel.","authors":"Yan-Qiu Wang, Li-Ming Wang, Li-Feng Han, Yi-Bing Chen, Yuan-Lu Cui","doi":"10.1016/j.jpha.2024.101102","DOIUrl":"10.1016/j.jpha.2024.101102","url":null,"abstract":"<p><p>Image 1.</p>","PeriodicalId":94338,"journal":{"name":"Journal of pharmaceutical analysis","volume":"15 5","pages":"101102"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12143808/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144251687","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Characterization of preclinical radio ADME properties of ARV-471 for predicting human PK using PBPK modeling. 利用PBPK模型对ARV-471临床前无线电ADME特性进行预测。
Journal of pharmaceutical analysis Pub Date : 2025-05-01 Epub Date: 2024-12-28 DOI: 10.1016/j.jpha.2024.101175
Yifei He, Chenggu Zhu, Peng Lei, Chen Yang, Yifan Zhang, Yuandong Zheng, Xingxing Diao
{"title":"Characterization of preclinical radio ADME properties of ARV-471 for predicting human PK using PBPK modeling.","authors":"Yifei He, Chenggu Zhu, Peng Lei, Chen Yang, Yifan Zhang, Yuandong Zheng, Xingxing Diao","doi":"10.1016/j.jpha.2024.101175","DOIUrl":"10.1016/j.jpha.2024.101175","url":null,"abstract":"<p><p>Proteolysis-targeting chimeras (PROTACs) represent a promising class of drugs that can target disease-causing proteins more effectively than traditional small molecule inhibitors can, potentially revolutionizing drug discovery and treatment strategies. However, the links between <i>in vitro</i> and <i>in vivo</i> data are poorly understood, hindering a comprehensive understanding of the absorption, distribution, metabolism, and excretion (ADME) of PROTACs. In this work, <sup>14</sup>C-labeled vepdegestrant (ARV-471), which is currently in phase III clinical trials for breast cancer, was synthesized as a model PROTAC to characterize its preclinical ADME properties and simulate its clinical pharmacokinetics (PK) by establishing a physiologically based pharmacokinetics (PBPK) model. For <i>in vitro</i>-<i>in vivo</i> extrapolation (IVIVE), hepatocyte clearance correlated more closely with <i>in vivo</i> rat PK data than liver microsomal clearance did. PBPK models, which were initially developed and validated in rats, accurately simulate ARV-471's PK across fed and fasted states, with parameters within 1.75-fold of the observed values. Human models, informed by <i>in vitro</i> ADME data, closely mirrored postoral dose plasma profiles at 30 mg. Furthermore, no human-specific metabolites were identified <i>in vitro</i> and the metabolic profile of rats could overlap that of humans. This work presents a roadmap for developing future PROTAC medications by elucidating the correlation between <i>in vitro</i> and <i>in vivo</i> characteristics.</p>","PeriodicalId":94338,"journal":{"name":"Journal of pharmaceutical analysis","volume":"15 5","pages":"101175"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12151198/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144268260","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Huangqin decoction inhibits colorectal inflammatory cancer transformation by improving gut microbiome-mediated metabolic dysfunction. 黄芩汤通过改善肠道微生物介导的代谢功能障碍抑制结直肠癌的转化。
Journal of pharmaceutical analysis Pub Date : 2025-05-01 Epub Date: 2024-11-04 DOI: 10.1016/j.jpha.2024.101138
Lu Lu, Yuan Li, Hang Su, Sisi Ren, Yujing Liu, Gaoxuan Shao, Weiwei Liu, Guang Ji, Hanchen Xu
{"title":"Huangqin decoction inhibits colorectal inflammatory cancer transformation by improving gut microbiome-mediated metabolic dysfunction.","authors":"Lu Lu, Yuan Li, Hang Su, Sisi Ren, Yujing Liu, Gaoxuan Shao, Weiwei Liu, Guang Ji, Hanchen Xu","doi":"10.1016/j.jpha.2024.101138","DOIUrl":"10.1016/j.jpha.2024.101138","url":null,"abstract":"<p><p>Colorectal inflammatory cancer transformation poses a major risk to patients with colitis. Patients with chronic intestinal inflammation have an approximately 2-3 folds increased risk of developing colorectal cancer (CRC). Unfortunately, there is currently no effective intervention available. Huangqin decoction (HQD), a well-known traditional Chinese medicine (TCM) formula, is frequently clinically prescribed for treating patients with colitis, and its active ingredients have effective antitumour efficacy. Nonetheless, the mechanism of HQD-mediated prevention of colorectal inflammatory cancer transformation remains unclear. A strategy integrating metagenomic, lipidomic, and messenger RNA (mRNA) sequencing analysis was used to investigate the regulatory effects of HQD on the gut microbiome, metabolism and potential mechanisms involved in colorectal inflammatory cancer transformation. Our study revealed that HQD suppressed colorectal inflammatory cancer transformation, which was associated with enhanced intestinal barrier function, decreased the inflammatory response, and regulation of the gut microbiome. Notably, cohousing experiments revealed that the transfer of the gut microbiome from HQD-treated mice largely inhibited the pathological transformation of colitis. Moreover, gut microbiome transfer from HQD-treated mice primarily resulted in the altered regulation of fatty acid metabolism, especially the remodeling of arachidonic acid metabolism, which was associated with the amelioration of pathological transformation. Arachidonic acid metabolism and the key metabolic enzyme arachidonic acid 12-lipoxygenase (ALOX12) were affected by HQD treatment, and no obvious protective effect of HQD was observed in <i>Alox</i> <i>12</i> <sup>-/-</sup> mice, which revealed that ALOX12 was a critical mediator of HQD protection against colorectal inflammatory cancer transformation. In summary, multiple omics analyses were applied to produce valuable data and theoretical support for the application of HQD as a promising intervention for the transformation of inflammatory CRC.</p>","PeriodicalId":94338,"journal":{"name":"Journal of pharmaceutical analysis","volume":"15 5","pages":"101138"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12153368/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144277279","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
A gene set enrichment analysis for cancer hallmarks. 癌症特征的基因集富集分析。
Journal of pharmaceutical analysis Pub Date : 2025-05-01 Epub Date: 2024-08-03 DOI: 10.1016/j.jpha.2024.101065
Otília Menyhart, William Jayasekara Kothalawala, Balázs Győrffy
{"title":"A gene set enrichment analysis for cancer hallmarks.","authors":"Otília Menyhart, William Jayasekara Kothalawala, Balázs Győrffy","doi":"10.1016/j.jpha.2024.101065","DOIUrl":"10.1016/j.jpha.2024.101065","url":null,"abstract":"<p><p>The \"hallmarks of cancer\" concept provides a valuable framework for understanding fundamental organizing principles common to various cancers. However, without a consensus gene set for cancer hallmarks, data comparison and integration result in diverse biological interpretations across studies. Therefore, we aimed to form a consensus cancer hallmark gene set by merging data from available mapping resources and establishing a framework for mining these gene sets. By consolidating data from seven projects, 6763 genes associated with 10 cancer hallmarks were identified. A cancer hallmarks enrichment analysis was performed for prognostic genes associated with overall survival across 12 types of solid tumors. \"Tissue invasion and metastasis\" was most prominent in cancers of the stomach (<i>P =</i> 2.2 × 10<sup>-11</sup>), pancreas (<i>P =</i> 4.2 × 10<sup>-9</sup>), bladder (<i>P =</i> 3.3 × 10<sup>-8</sup>), and ovaries (<i>P =</i> 0.0007), aligning with their heightened potential to spread. \"Sustained angiogenesis\" was most prominent in squamous cell carcinomas of the lung (<i>P =</i> 2.5 × 10<sup>-7</sup>), while \"genome instability\" showed strong enrichment in lung adenocarcinomas (LUADs) (<i>P =</i> 1.5 × 10<sup>-8</sup>) and cancers of the liver (<i>P =</i> 5.5 × 10<sup>-10</sup>), pancreas (<i>P =</i> 2.1 × 10<sup>-5</sup>), and kidney (<i>P</i> = 0.018). Pancreatic cancers displayed the highest enrichment of hallmarks, emphasizing the disease's complexity, while in melanomas and cancers of the liver, prostate, and kidney, a single hallmark was enriched among the prognostic markers of survival. Additionally, an online tool (www.cancerhallmarks.com) that allows the identification of cancer-associated hallmarks from new gene sets was established. In summary, our aim of establishing a consensus list of cancer hallmark genes was achieved. Furthermore, the analysis of survival-associated genes revealed a unique pattern of hallmark enrichment with potential pharmacological implications in different tumor types.</p>","PeriodicalId":94338,"journal":{"name":"Journal of pharmaceutical analysis","volume":"15 5","pages":"101065"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12151186/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144268256","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
An improved reporter gene assay for evaluating the biological activity of recombinant human growth hormone. 一种评价重组人生长激素生物活性的改进报告基因试验。
Journal of pharmaceutical analysis Pub Date : 2025-05-01 Epub Date: 2024-08-18 DOI: 10.1016/j.jpha.2024.101073
Xiaoming Zhang, Heyang Li, Ying Huang, Ping Lv, Lvyin Wang, Kezheng Xu, Yi Li, Xinyue Hu, Yue Sun, Cheng-Gang Liang, Jing Li
{"title":"An improved reporter gene assay for evaluating the biological activity of recombinant human growth hormone.","authors":"Xiaoming Zhang, Heyang Li, Ying Huang, Ping Lv, Lvyin Wang, Kezheng Xu, Yi Li, Xinyue Hu, Yue Sun, Cheng-Gang Liang, Jing Li","doi":"10.1016/j.jpha.2024.101073","DOIUrl":"10.1016/j.jpha.2024.101073","url":null,"abstract":"<p><p>Image 1.</p>","PeriodicalId":94338,"journal":{"name":"Journal of pharmaceutical analysis","volume":"15 5","pages":"101073"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12150084/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144268259","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Exploring cellular plasticity and resistance mechanisms in lung cancer: Innovations and emerging therapies. 探索肺癌的细胞可塑性和耐药机制:创新和新兴疗法。
Journal of pharmaceutical analysis Pub Date : 2025-05-01 Epub Date: 2025-01-03 DOI: 10.1016/j.jpha.2024.101179
Caiyu Jiang, Shenglong Xie, Kegang Jia, Gang Feng, Xudong Ren, Youyu Wang
{"title":"Exploring cellular plasticity and resistance mechanisms in lung cancer: Innovations and emerging therapies.","authors":"Caiyu Jiang, Shenglong Xie, Kegang Jia, Gang Feng, Xudong Ren, Youyu Wang","doi":"10.1016/j.jpha.2024.101179","DOIUrl":"10.1016/j.jpha.2024.101179","url":null,"abstract":"<p><p>Non-small cell lung cancer (NSCLC) accounts for the majority of lung cancer cases and remains the leading cause of cancer-related mortality worldwide. Firstly, this review explores the limitations of conventional therapies, chemotherapy, radiotherapy, and surgery, focusing on the development of drug resistance and significant toxicity that often hinder their efficacy. Thereafter, advancements in targeted therapies, such as immune checkpoint inhibitors (ICIs) and tyrosine kinase inhibitors (TKIs), are discussed, highlighting their impact on improving outcomes for patients with specific genetic mutations, including c-ros oncogene 1 receptor tyrosine kinase (ROS1), anaplastic lymphoma kinase (ALK), and epidermal growth factor receptor (EGFR). Additionally, the emergence of novel immunotherapies and phytochemicals is examined, emphasizing their potential to overcome therapeutic resistance, particularly in advanced-stage diseases. The review also delves into the role of next-generation sequencing (NGS) in enabling personalized treatment approaches and explores the clinical potential of innovative agents, such as bispecific T-cell engagers (BiTEs) and antibody-drug conjugates (ADCs). Finally, we address the socioeconomic barriers that limit the accessibility of these therapies in low-resource settings and propose future research directions aimed at improving the long-term efficacy and accessibility of these treatments.</p>","PeriodicalId":94338,"journal":{"name":"Journal of pharmaceutical analysis","volume":"15 5","pages":"101179"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12151197/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144268261","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Inhibiting neddylation: A new strategy for tumor therapy. 抑制类化修饰:肿瘤治疗的新策略。
Journal of pharmaceutical analysis Pub Date : 2025-05-01 Epub Date: 2024-11-08 DOI: 10.1016/j.jpha.2024.101140
Jian Sun, Cui Liu, Changhui Lang, Jing Wang, Qingxiang Li, Chang Peng, Zuochen Du, Yan Chen, Pei Huang
{"title":"Inhibiting neddylation: A new strategy for tumor therapy.","authors":"Jian Sun, Cui Liu, Changhui Lang, Jing Wang, Qingxiang Li, Chang Peng, Zuochen Du, Yan Chen, Pei Huang","doi":"10.1016/j.jpha.2024.101140","DOIUrl":"10.1016/j.jpha.2024.101140","url":null,"abstract":"<p><p>Neddylation is a crucial posttranslational modification that involves the attachment of neural precursor cell-expressed developmentally downregulated protein 8 (NEDD8) to a lysine residue in the substrate via the sequential actions of the E1 NEDD8-activating enzyme (NAE) (E1), E2 NEDD8-conjugating enzyme (E2), and E3 NEDD8-ligase (E3). The most extensively studied substrates of neddylation are members of the cullin family, which act as scaffold components for cullin ring E3 ubiquitin ligases (CRLs). Since cullin neddylation activates CRLs, which are frequently overactive in tumors, inhibiting neddylation has emerged as a promising strategy for developing novel antitumor therapies. This review explores the antitumor effects of inhibiting neddylation that leads to the inactivation of CRLs and provides a summary of known inhibitors that target protein-protein interactions (PPIs) within the neddylation enzymatic cascade.</p>","PeriodicalId":94338,"journal":{"name":"Journal of pharmaceutical analysis","volume":"15 5","pages":"101140"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12151199/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144268262","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","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 final stretch of the animal-free approach in new drug research. 新药研究中无动物实验的最后一步。
Journal of pharmaceutical analysis Pub Date : 2025-05-01 Epub Date: 2025-05-15 DOI: 10.1016/j.jpha.2025.101344
Li Liu
{"title":"The final stretch of the animal-free approach in new drug research.","authors":"Li Liu","doi":"10.1016/j.jpha.2025.101344","DOIUrl":"https://doi.org/10.1016/j.jpha.2025.101344","url":null,"abstract":"","PeriodicalId":94338,"journal":{"name":"Journal of pharmaceutical analysis","volume":"15 5","pages":"101344"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12151227/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144268266","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Impact of FASN-enriched EVs on endothelial cell function in obstructive sleep apnea hypopnea syndrome. fasn富集的ev对阻塞性睡眠呼吸暂停低通气综合征内皮细胞功能的影响。
Journal of pharmaceutical analysis Pub Date : 2025-05-01 Epub Date: 2025-03-01 DOI: 10.1016/j.jpha.2025.101251
Yuan Tian, Dan Zhang, Huaian Yang, Xiaoli Zhang, Shengqun Xu
{"title":"Impact of FASN-enriched EVs on endothelial cell function in obstructive sleep apnea hypopnea syndrome.","authors":"Yuan Tian, Dan Zhang, Huaian Yang, Xiaoli Zhang, Shengqun Xu","doi":"10.1016/j.jpha.2025.101251","DOIUrl":"10.1016/j.jpha.2025.101251","url":null,"abstract":"<p><p>Endothelial dysfunction is a key factor linking obstructive sleep apnea hypopnea syndrome (OSAHS) with cardiovascular diseases. In this study, we used advanced proteomics and metabolomics approaches to investigate the impact of extracellular vesicles (EVs) derived from the serum of OSAHS patients on endothelial function. Our multi-omics analysis identified dysregulated pathways related to fatty acid metabolism, apoptosis regulation, and inflammatory responses, highlighting fatty acid synthase (FASN) as a crucial player in OSAHS-induced endothelial dysfunction. Both <i>in vitro</i> and <i>in vivo</i> experiments demonstrated that FASN-enriched EVs impair endothelial cell viability and disrupt metabolic homeostasis, offering new insights for the development of targeted therapies for cardiovascular complications associated with OSAHS.</p>","PeriodicalId":94338,"journal":{"name":"Journal of pharmaceutical analysis","volume":"15 5","pages":"101251"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12166414/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144304261","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Screen of FDA-approved drug library identifies vitamin K as anti-ferroptotic drug for osteoarthritis therapy through Gas6. fda批准的药物文库筛选发现维生素K是通过Gas6治疗骨关节炎的抗铁张力药物。
Journal of pharmaceutical analysis Pub Date : 2025-05-01 Epub Date: 2024-08-29 DOI: 10.1016/j.jpha.2024.101092
Yifeng Shi, Sunlong Li, Shuhao Zhang, Caiyu Yu, Jiansen Miao, Shu Yang, Yan Chen, Yuxuan Zhu, Xiaoxiao Huang, Chencheng Zhou, Hongwei Ouyang, Xiaolei Zhang, Xiangyang Wang
{"title":"Screen of FDA-approved drug library identifies vitamin K as anti-ferroptotic drug for osteoarthritis therapy through Gas6.","authors":"Yifeng Shi, Sunlong Li, Shuhao Zhang, Caiyu Yu, Jiansen Miao, Shu Yang, Yan Chen, Yuxuan Zhu, Xiaoxiao Huang, Chencheng Zhou, Hongwei Ouyang, Xiaolei Zhang, Xiangyang Wang","doi":"10.1016/j.jpha.2024.101092","DOIUrl":"10.1016/j.jpha.2024.101092","url":null,"abstract":"<p><p>Ferroptosis of chondrocytes is a significant contributor to osteoarthritis (OA), for which there is still a lack of safe and effective therapeutic drugs targeting ferroptosis. Here, we screen for anti-ferroptotic drugs in Food and Drug Administration (FDA)-approved drug library <i>via</i> a high-throughput manner in chondrocytes. We identified a group of FDA-approved anti-ferroptotic drugs, among which vitamin K showed the most powerful protective effect. Further study demonstrated that vitamin K effectively inhibited ferroptosis and alleviated the extracellular matrix (ECM) degradation in chondrocytes. Intra-articular injection of vitamin K inhibited ferroptosis and alleviated OA phenotype in destabilization of the medial meniscus (DMM) mouse model. Mechanistically, transcriptome sequencing and knockdown experiments revealed that the anti-ferroptotic effects of vitamin K depended on growth arrest-specific 6 (Gas6). Furthermore, exogenous expression of Gas6 was found to inhibit ferroptosis through the AXL receptor tyrosine kinase (AXL)/phosphatidylinositol 3-kinase (PI3K)/AKT serine/threonine kinase (AKT) axis. Together, we demonstrate that vitamin K inhibits ferroptosis and alleviates OA progression <i>via</i> enhancing Gas6 expression and its downstream pathway of AXL/PI3K/AKT axis, indicating vitamin K as well as Gas6 to serve as a potential therapeutic target for OA and other ferroptosis-related diseases.</p>","PeriodicalId":94338,"journal":{"name":"Journal of pharmaceutical analysis","volume":"15 5","pages":"101092"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12151230/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144268265","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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