沉默信息调节因子3通过调节线粒体功能障碍减轻特发性肺纤维化的研究进展  

Progress in role of silent information regulator 3 in improving idiopathic pulmonary fibrosis by regulating mitochondrial dysfunction

作　　者：杨树森 刘禹杉 张仪霖 惠毅[1] 李京涛 闫曙光[1,2] YANG Shusen;LIU Yushan;ZHANG Yilin;HUI Yi;LI Jingtao;YAN Shuguang(Basic Medical College of Shaanxi University of Chinese Medicine,Xianyang 712046,China;Key Laboratory of Prescrip-tions and Medicines for Gastrointestinal Diseases in Shaanxi Province,Xianyang 712046,China;Affiliated Hospital of Shaanxi University of Chinese Medicine,Xianyang 712000,China)

机构地区：[1]陕西中医药大学基础医学院,陕西咸阳712046 [2]陕西省胃肠病证方药重点研究室,陕西咸阳712046 [3]陕西中医药大学附属医院,陕西咸阳712000

出　　处：《中国病理生理杂志》2024年第2期358-364,共7页Chinese Journal of Pathophysiology

基　　金：国家自然科学基金资助项目(No.81703974)。

摘　　要：特发性肺纤维化(idiopathic pulmonary fibrosis,IPF)是一种以进行性肺瘢痕形成为主要特征慢性进行性肺部疾病[1]。IPF属于典型且常见的纤维性间质性肺病,其病理进程不可逆转,往往会进展为呼吸衰竭和死亡[2],确诊后的平均预期寿命为3~5年[3]。抗纤维化药物pirfenidone和nintedanib可以改善IPF患者的肺功能,但其疗效不佳且副作用较大[4]。Idiopathic pulmonary fibrosis(IPF)is a chronic progressive interstitial lung disease of unknown etiology,with a rapid disease course,poor prognosis,and the absence of effective therapeutic drugs.Mitochondrial dysfunction is one of the crucial causes of inducing IPF.Silent information regulator 3(SIRT3)can restore mitochondrial homeostasis by inhibiting mitochondrial oxidative stress,repairing mitochondrial DNA damage,and ameliorating abnormal mitochondrial lipid metabolism.This paper summarizes the role and mechanism of SIRT3 in attenuating mitochondrial dysfunction based on delineating the relationship between mitochondrial dysfunction and IPF,aiming to provide references for finding effective treatment methods for IPF.

关 键 词：特发性肺纤维化 线粒体功能障碍 沉默信息调节因子3 DNA损伤 脂质代谢 

分 类 号：R563[医药卫生—呼吸系统] R363[医药卫生—内科学] Q591.5[医药卫生—临床医学]