JQ1 is a potential therapeutic option for COPD patients with agrin overexpression

Am J Physiol Lung Cell Mol Physiol. 2018 Apr 1;314(4):L690-L694. doi: 10.1152/ajplung.00500.2017. Epub 2017 Dec 28.


Chronic obstructive pulmonary disease (COPD) is one of the leading causes of morbidity and death worldwide. It is characterized by chronic pulmonary inflammation and obstructed airflow from the lungs. To date, there is no effective treatment for COPD. The activation of the agrin (AGRN-YAP pathway can promote heart regeneration. Because agrin can induce only mild cardiomyocyte proliferation compared with ERBB2 pathway activation, it might exert pleiotropic effects, such as mitigation of innate inflammation, immune response, and fibrosis. Previously, we demonstrated that several common pathological gene regulatory programs such as innate inflammatory and profibrotic transcriptional networks were shared by COPD and heart failure. In this study, we show that agrin is inversely correlated with COPD development and progression and may exert its effects by suppressing innate inflammation and profibrotic signaling pathways. BET inhibitor JQ1, in line with our previous findings, is a promising therapeutic option in the treatment of patients with COPD. Nevertheless, wet laboratory experiments and clinical trials are needed before its application in clinical practice.

Keywords: agrin; chronic obstructive pulmonary disease; inflammation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Agrin / antagonists & inhibitors
  • Agrin / metabolism*
  • Azepines / pharmacology*
  • Biomarkers / metabolism*
  • Computational Biology / methods*
  • Female
  • Humans
  • Male
  • Middle Aged
  • Pulmonary Disease, Chronic Obstructive / drug therapy*
  • Pulmonary Disease, Chronic Obstructive / metabolism*
  • Pulmonary Disease, Chronic Obstructive / pathology
  • Triazoles / pharmacology*


  • (+)-JQ1 compound
  • Agrin
  • Azepines
  • Biomarkers
  • Triazoles