{"title":"Expression and Effects of FUS/Sfrp5/Wnt5 in Atherosclerosis Development.","authors":"Xiaogao Wang, Hui Wang, Ran Lu, Shiyuan Chen, Yong Gao, Chaowen Yu","doi":"","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>Atherosclerosis (AS) contributes significantly to the development of cardiovascular disease. Despite recent advances in medical treatment, the outcomes for patients with AS are still unsatisfactory. This study aims to enhance our understanding of AS and pave the way for the development of more effective therapeutic approaches to improve patient outcomes and ultimately reduce the burden of this devastating condition.</p><p><strong>Methods: </strong>An AS cell model was established using oxidized low-density lipoprotein (OX-LDL) administration to human vascular smooth muscle cells (HVSMCs), followed by injection with oe-NC, oe-FUS, oe-Sfrp5, or oe-FUS+ oe-Sfrp5. Western blot, Transwell assay, CCK8 assay, Oil Red O staining assay, and ELISA were used to elucidate the mechanisms of the FUS/Sfrp5/Wnt5 pathway in our model of AS.</p><p><strong>Results: </strong>In this study, both FUS and Sfrp5 inhibited Wnt5a expression. In addition, FUS inhibited lipid droplet formation and migration capacity of OX-LDL-induced HVSMCs, and FUS and Sfrp5 may have a synergistic effect in controlling Wnt5a in AS. These results highlight the potential therapeutic value of targeting the FUS and Sfrp5 pathway to control AS progression.</p><p><strong>Conclusion: </strong>The findings suggest that FUS and Sfrp5 may have a synergistic effect in controlling Wnt5a in AS.</p>","PeriodicalId":8228,"journal":{"name":"Annals of clinical and laboratory science","volume":"55 2","pages":"240-246"},"PeriodicalIF":1.1000,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Annals of clinical and laboratory science","FirstCategoryId":"3","ListUrlMain":"","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"MEDICAL LABORATORY TECHNOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Objective: Atherosclerosis (AS) contributes significantly to the development of cardiovascular disease. Despite recent advances in medical treatment, the outcomes for patients with AS are still unsatisfactory. This study aims to enhance our understanding of AS and pave the way for the development of more effective therapeutic approaches to improve patient outcomes and ultimately reduce the burden of this devastating condition.
Methods: An AS cell model was established using oxidized low-density lipoprotein (OX-LDL) administration to human vascular smooth muscle cells (HVSMCs), followed by injection with oe-NC, oe-FUS, oe-Sfrp5, or oe-FUS+ oe-Sfrp5. Western blot, Transwell assay, CCK8 assay, Oil Red O staining assay, and ELISA were used to elucidate the mechanisms of the FUS/Sfrp5/Wnt5 pathway in our model of AS.
Results: In this study, both FUS and Sfrp5 inhibited Wnt5a expression. In addition, FUS inhibited lipid droplet formation and migration capacity of OX-LDL-induced HVSMCs, and FUS and Sfrp5 may have a synergistic effect in controlling Wnt5a in AS. These results highlight the potential therapeutic value of targeting the FUS and Sfrp5 pathway to control AS progression.
Conclusion: The findings suggest that FUS and Sfrp5 may have a synergistic effect in controlling Wnt5a in AS.
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