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放射性心肌纤维化是放射性心脏损伤(radiation-induced heart disease,RIHD)的重要病理过程,可导致心脏功能下降、心肌重塑等,影响患者生存质量。既往多位学者在细胞、分子、基因等层面对此进行了研究,一般认为是纤维母细胞异常分化、微血管内皮损伤、炎症、氧化应激反应、转化生长因子-β1(TGF-β1)信号转导、基因表达改变等多种因子及信号通路相互作用的结果,但分子生物学机制错综复杂,仍未完全明确,目前尚无有效的临床干预措施。本文旨在探讨RIHD心肌纤维化的发生机制及临床干预措施,并对其新进展、面临的挑战以及未来的发展方向做一概述。
Radioactive myocardial fibrosis is an important pathological process of radiation-induced heart disease (RIHD), which can lead to the decline of cardiac function and myocardial remodeling, which affects the quality of life of patients. Many scholars in the past have carried out researches on the aspects of cell, molecule and gene, which are generally considered as abnormal differentiation of fibroblasts, microvascular endothelial injury, inflammation, oxidative stress reaction, transforming growth factor-β1 (TGF-β1) signaling Guide, gene expression changes and other factors and signal pathway interaction results, but the molecular biology mechanism is complex and not yet fully clear, there is no effective clinical intervention. This article aims to explore the mechanism of RIHD myocardial fibrosis and clinical interventions, and its new progress, challenges and future directions to make an overview.