{"title":"Radiation-induced vascular damage and aging: a review of potential therapeutic targets and key signaling pathways","authors":"Chen Li , Liqiu Ma","doi":"10.1016/j.radmp.2025.04.003","DOIUrl":null,"url":null,"abstract":"<div><div>Radiation-induced vascular damage has attracted significant attention in various fields, including healthcare (radiotherapy), the nuclear industry (nuclear facilities and devices), and space exploration. Recent studies have indicated a close relationship between such damage and aging, involving multiple signaling pathways and biological targets. This review aims to summarize the potential mechanisms underlying radiation-induced vascular damage, explore key molecular targets and related signaling pathways during the aging process, and provide a theoretical foundation for developing future therapeutic strategies. The review discusses direct mechanisms of radiation-induced vascular damage, such as apoptosis, necrosis, endothelial dysfunction, and alterations in the extracellular matrix. It also delves into the biological links between vascular damage and aging, including changes in the expression of aging markers, telomere shortening, and immune responses. Key molecular targets, such as the p53 pathway, nuclear factor-kappa B (NF-κB) signaling pathway, and silent information regulator 2-related enzyme 1 (SIRT1), are examined for their roles in mediating vascular damage and aging. Additionally, major signaling pathways such as MAPK, PI3K/Akt, and Wnt/β-catenin are analyzed for their involvement in cellular stress responses and vascular repair mechanisms. The review also summarizes the evaluation of current clinical treatments, discusses the potential therapeutic value of new targets, and outlines future research directions and challenges in the field.</div></div>","PeriodicalId":34051,"journal":{"name":"Radiation Medicine and Protection","volume":"6 3","pages":"Pages 140-146"},"PeriodicalIF":0.0000,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Radiation Medicine and Protection","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S2666555725000449","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"Health Professions","Score":null,"Total":0}
引用次数: 0
Abstract
Radiation-induced vascular damage has attracted significant attention in various fields, including healthcare (radiotherapy), the nuclear industry (nuclear facilities and devices), and space exploration. Recent studies have indicated a close relationship between such damage and aging, involving multiple signaling pathways and biological targets. This review aims to summarize the potential mechanisms underlying radiation-induced vascular damage, explore key molecular targets and related signaling pathways during the aging process, and provide a theoretical foundation for developing future therapeutic strategies. The review discusses direct mechanisms of radiation-induced vascular damage, such as apoptosis, necrosis, endothelial dysfunction, and alterations in the extracellular matrix. It also delves into the biological links between vascular damage and aging, including changes in the expression of aging markers, telomere shortening, and immune responses. Key molecular targets, such as the p53 pathway, nuclear factor-kappa B (NF-κB) signaling pathway, and silent information regulator 2-related enzyme 1 (SIRT1), are examined for their roles in mediating vascular damage and aging. Additionally, major signaling pathways such as MAPK, PI3K/Akt, and Wnt/β-catenin are analyzed for their involvement in cellular stress responses and vascular repair mechanisms. The review also summarizes the evaluation of current clinical treatments, discusses the potential therapeutic value of new targets, and outlines future research directions and challenges in the field.