Chemokine CCL1 as a therapeutic target for pulmonary fibrosis: comments on ‘The chemokine CCL1 triggers an AMFR‒SPRY1 pathway that promotes differentiation of lung fibroblasts into myofibroblasts and drives pulmonary fibrosis’  

作　　者：Shanshan Liu Chang Liu Zhuowei Hu Yang Xiao 

机构地区：[1]National Clinical Research Center for Metabolic Diseases,Key Laboratory of Diabetes Immunology,Ministry of Education,and Department of Metabolism and Endocrinology,The Second Xiangya Hospital of Central South University,Changsha 410011,Hunan,China [2]Drug Clinical Trial Institution,Children’s Hospital,Capital Institute of Pediatrics,Beijing 100020,China

出　　处：《Journal of Molecular Cell Biology》2022年第1期65-66,共2页分子细胞生物学报（英文版）

基　　金：The work described was supported by grants from the National Key R&D Program of China(2018YFE0114500);the‘361 Project’Outstanding Young Talent of the Second Xiangya Hospital of Central South University,the National Natural Science Foundation of China(81803604);the National Science Foundation of Hunan Province for Excellent Young Scholars(2020JJ3056).

摘　　要：Pulmonary fibrosis(PF)is a type of chronic and progressive respiratory diseases characterized by excessive extracellular matrix(ECM)deposition,interstitial fibrotic lesions,and architectural distortion.Patients with PF suffer from pulmonary function decline and progressive worsening of dyspnea with poor prognosis(Wilson and Wynn,2009).Although recent progress provides mechanistic insights into the pathogenesis of PF,no effective treatment against PF is available other than lung transplantation.Therefore,a better understanding of the molecular and cellular mechanisms of PF is crucial for the discovery of new therapeutic targets for safe and effective anti-PF drugs.

关 键 词：THERAPEUTIC lung DRUGS 

分 类 号：R563[医药卫生—呼吸系统]