医学
氯沙坦
癌症研究
肺纤维化
血管紧张素II
纤维化
小RNA
氧化应激
衰老
机制(生物学)
SMAD公司
PTEN公司
信号转导
药理学
生物信息学
转化生长因子
生物
细胞生物学
内科学
PI3K/AKT/mTOR通路
受体
生物化学
哲学
认识论
基因
作者
Pataje G.S. Prasanna,Molykutty J. Aryankalayil,Deborah E. Citrin,C. Norman Coleman
标识
DOI:10.1080/09553002.2023.2177768
摘要
Purpose Progressive, irreversible radiation-induced pulmonary fibrosis (RIPF) is a clinically significant intermediate- to a late-occurring side effect of radiotherapy. Known mechanisms of RIPF include oxidative stress-induced activation of TGF-β with activation of SMAD signaling, TNF-α elaboration, and activation of the Angiotensin Converting Enzyme (ACE) mediated production of angiotensin II with resulting activation of profibrotic cytokine signaling and vasoconstriction. The pioneering work of John Moulder, to whom this paper is dedicated, and several of his colleagues demonstrated that inhibiting the conversion of ACE with drugs such as Captopril, Enalapril, and Losartan can ameliorate radiation fibrosis in various tissues. While this work led several groups to probe mechanism-based pharmacological mitigation of RIPF, in this article, we explore and discuss the roles of microRNAs (miRNA) and therapy-induced senescence (TIS) in the pathogenesis of and potential biomarkers for RIPF.Conclusion Our analysis of the published literature in the last decade on RIPF, miRNA, and TIS identifies TIS as a mechanism in the onset and progression of RIPF, which is regulated through several miRNAs. This work may lead to the discovery and development of the next generation of miRNA therapeutics and/or the repurposing of approved pharmaceutical agents and the development of early biomarker panels to predict RIPF.
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