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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’
Shanshan Liu1,* , Chang Liu2 , Zhuowei Hu1 , Yang Xiao1,*
1National 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
2Drug Clinical Trial Institution, Children’s Hospital, Capital Institute of Pediatrics, Beijing 100020, China
*Correspondence to:Shanshan Liu , Email:lss0625@csu.edu.cn Yang Xiao , Email:xiaoyang29@csu.edu.cn
J Mol Cell Biol, Volume 14, Issue 1, January 2022, mjab080,  https://doi.org/10.1093/jmcb/mjab080

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.