{"title":"抑制磷酸甘油酸激酶1 (PGK1)可减少贴片血管成形术后新生内膜增生。","authors":"Peng Sun, Hao Cui, Changwei Ren, Chenzhen Xu, Chuanjie Yue, Jing'an Li, Yongqiang Lai","doi":"10.1021/acsabm.5c00589","DOIUrl":null,"url":null,"abstract":"<p><p>Neointimal hyperplasia is a known complication following aorta interventions. In this study, our hypothesis was that inhibiting phosphoglycerate kinase 1 (PGK1) could effectively reduce aortic neointimal hyperplasia in a rat model of abdominal aortic patch angioplasty. The role of the glycolytic pathway in patch angioplasty was analyzed by next-generation sequencing data, and the core role of PGK1 was found by differential gene analysis. The rats were allocated into two distinct groups: a control group that did not receive any supplementary treatment and a group treated with NG52, an inhibitor of PGK1, which was administered via a PLGA coating. Abdominal aortic patches were surgically implanted in the rats and subsequently harvested on the 14th day postimplantation for further analysis. Immunohistochemical analysis identified the presence of PGK1-positive cells within the neointima of the rat model subjected to abdominal aortic patch angioplasty. Importantly, the use of NG52 PLGA coating significantly decreased neointimal thickness (<i>p</i> < 0.0001). The mechanism of action of NG52 may involve the inhibition of TGFβ1 expression and the activation of the signaling pathway. Consequently, targeting the PGK1 pathway holds promise as a therapeutic strategy to mitigate aortic neointimal hyperplasia.</p>","PeriodicalId":2,"journal":{"name":"ACS Applied Bio Materials","volume":" ","pages":"5930-5937"},"PeriodicalIF":4.6000,"publicationDate":"2025-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Inhibition of Phosphoglycerate Kinase 1 (PGK1) Decreases Neointimal Hyperplasia after Patch Angioplasty.\",\"authors\":\"Peng Sun, Hao Cui, Changwei Ren, Chenzhen Xu, Chuanjie Yue, Jing'an Li, Yongqiang Lai\",\"doi\":\"10.1021/acsabm.5c00589\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Neointimal hyperplasia is a known complication following aorta interventions. In this study, our hypothesis was that inhibiting phosphoglycerate kinase 1 (PGK1) could effectively reduce aortic neointimal hyperplasia in a rat model of abdominal aortic patch angioplasty. The role of the glycolytic pathway in patch angioplasty was analyzed by next-generation sequencing data, and the core role of PGK1 was found by differential gene analysis. The rats were allocated into two distinct groups: a control group that did not receive any supplementary treatment and a group treated with NG52, an inhibitor of PGK1, which was administered via a PLGA coating. Abdominal aortic patches were surgically implanted in the rats and subsequently harvested on the 14th day postimplantation for further analysis. Immunohistochemical analysis identified the presence of PGK1-positive cells within the neointima of the rat model subjected to abdominal aortic patch angioplasty. Importantly, the use of NG52 PLGA coating significantly decreased neointimal thickness (<i>p</i> < 0.0001). The mechanism of action of NG52 may involve the inhibition of TGFβ1 expression and the activation of the signaling pathway. Consequently, targeting the PGK1 pathway holds promise as a therapeutic strategy to mitigate aortic neointimal hyperplasia.</p>\",\"PeriodicalId\":2,\"journal\":{\"name\":\"ACS Applied Bio Materials\",\"volume\":\" \",\"pages\":\"5930-5937\"},\"PeriodicalIF\":4.6000,\"publicationDate\":\"2025-07-21\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"ACS Applied Bio Materials\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1021/acsabm.5c00589\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2025/6/17 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q2\",\"JCRName\":\"MATERIALS SCIENCE, BIOMATERIALS\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"ACS Applied Bio Materials","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1021/acsabm.5c00589","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/6/17 0:00:00","PubModel":"Epub","JCR":"Q2","JCRName":"MATERIALS SCIENCE, BIOMATERIALS","Score":null,"Total":0}
Inhibition of Phosphoglycerate Kinase 1 (PGK1) Decreases Neointimal Hyperplasia after Patch Angioplasty.
Neointimal hyperplasia is a known complication following aorta interventions. In this study, our hypothesis was that inhibiting phosphoglycerate kinase 1 (PGK1) could effectively reduce aortic neointimal hyperplasia in a rat model of abdominal aortic patch angioplasty. The role of the glycolytic pathway in patch angioplasty was analyzed by next-generation sequencing data, and the core role of PGK1 was found by differential gene analysis. The rats were allocated into two distinct groups: a control group that did not receive any supplementary treatment and a group treated with NG52, an inhibitor of PGK1, which was administered via a PLGA coating. Abdominal aortic patches were surgically implanted in the rats and subsequently harvested on the 14th day postimplantation for further analysis. Immunohistochemical analysis identified the presence of PGK1-positive cells within the neointima of the rat model subjected to abdominal aortic patch angioplasty. Importantly, the use of NG52 PLGA coating significantly decreased neointimal thickness (p < 0.0001). The mechanism of action of NG52 may involve the inhibition of TGFβ1 expression and the activation of the signaling pathway. Consequently, targeting the PGK1 pathway holds promise as a therapeutic strategy to mitigate aortic neointimal hyperplasia.
期刊介绍:
ACS Applied Bio Materials is an interdisciplinary journal publishing original research covering all aspects of biomaterials and biointerfaces including and beyond the traditional biosensing, biomedical and therapeutic applications.
The journal is devoted to reports of new and original experimental and theoretical research of an applied nature that integrates knowledge in the areas of materials, engineering, physics, bioscience, and chemistry into important bio applications. The journal is specifically interested in work that addresses the relationship between structure and function and assesses the stability and degradation of materials under relevant environmental and biological conditions.