PRACTICAL ONCOLOGY JOURNAL ›› 2015, Vol. 29 ›› Issue (1): 73-77.doi: 10.11904/j.issn.1002-3070.2015.01.016

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Progress on the mechanisms of antifibrotic effects of PPARγ

SUN Yunan,DUAN Qiongyu,WU Rong   

  1. Department of Oncology Secfion Ⅱ,Shengjing Hospital of China Medical University,Shenyang 110022,China
  • Received:2014-08-12 Online:2015-02-28 Published:2015-03-06

Abstract: External beam radiotherapy is a major treatment in the management of cancer.However radiation induced pulmonary fibrosis is common.It not only leads to quality-of-life issues in survivors and compromise treatment,but also may even be lethal in outcome.Transforming growth factor β(TGF-β)seems to be a key mediator of fibrosis.TGF-β promotes the differentiation of fibroblasts into myofibroblasts while the differentiation and activation of fibroblasts and myofibroblastsmay produce the components of scar tissue,which is one of the key pathogenic processes in lung fibrosis.Peroxisome proliferator activated receptors(PPARs)are ligand activated transcription factors that belong to the nuclear hormone receptor superfamily.PPARγ is also a key regulator of fibroblast differentiation.Many studies have shown that both natural ligand and synthetic ligand of PPARγ can suppress fibrosis by interfering with TGF-β signaling and some other approaches.The antifibrotic effects of PPARγ have been reported to be involved in both PPARγ dependent and PPARγ independent mechanisms.PPARγ agonists may have potential for the therapy of radiation induced pulmonary fibrosis.

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