文献类型：期刊文献

中文题名：高原适应基因PPARA和慢性阻塞性肺疾病发病机制相关性研究概述

英文题名：Summary of studies on the correlation between altitude adaptation gene PPARA and pathogenesis of chronic obstructive pulmonary disease

作者：王啟秀[1];王云超[2];余静[1];张春艳[1];王新华[1]

第一作者：王啟秀

机构：[1]甘肃中医药大学公共卫生学院,兰州730000;[2]甘肃中医药大学基础医学院,兰州730000

第一机构：甘肃中医药大学公共卫生学院

年份：2023

卷号：43

期号：4

起止页码：486

中文期刊名：国际呼吸杂志

外文期刊名：International Journal of Respiration

收录：CSTPCD

基金：国家重点研发计划(2017YFC0907202)。

语种：中文

中文关键词：肺疾病,慢性阻塞性;低氧;PPARA基因;高原适应

外文关键词：Pulmonary disease,chronic obstructive;Hypoxia;Peroxisome proliferator-activated receptor alpha genes;Plateau

摘要：慢性阻塞性肺疾病(COPD)是以不可逆的气流受限为主要特征的具有较高发病率的疾病,炎症机制是目前较为公认的发病机制。过氧化物酶体增殖物激活受体α基因PPARA基因能够使藏族人群在高原环境下血红蛋白浓度低于其他人群,在适应缺氧环境中发挥重要的作用,并且该基因编码的过氧化物酶体增殖物激活受体α与提高氧的利用率、保证缺氧条件下的能量供应和抑制炎症有关。COPD的发生与炎症机制关系密切,患者会出现不同程度的缺氧表现,因此推测COPD的炎症机制或许与PPARA基因有关。本文通过简述PPARA基因与过氧化物酶体增殖物激活受体α在高原适应中的作用,探讨PPARA基因与COPD炎症机制的联系,寻找高原缺氧环境中与COPD发病相关的基因,为后续COPD发病机制的研究提供新的思路。
Chronic obstructive pulmonary disease(COPD)is a disease characterized by irreversible airflow restriction with a high incidence,and the inflammatory mechanism is currently recognized as the pathogenesis.Peroxisome proliferator-activated receptor alpha gene,PPARA gene,can make Tibetans′hemoglobin concentration lower than other people in the plateau environment,which plays an important role in adapting to the hypoxia environment.Moreover,PPARA encoded by this gene is related to improving the utilization rate of oxygen,ensuring energy supply under hypoxia,and inhibiting inflammation.The occurrence of COPD is closely related to the inflammatory mechanism,and patients will suffer different degrees of hypoxia.Therefore,it is speculated that the inflammatory mechanism of COPD may be related to the PPARA gene.In this paper,the role of PPARA gene and PPARαin altitude adaptation was briefly described and the relationship between PPARA gene and the mechanism of COPD was explored,so as to find the genes related to the pathogenesis of COPD in the altitude hypoxia environment,finally to provide new ideas for the follow-up study of the pathogenesis of COPD.