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PPARγ抗肺纤维化机制的研究进展 被引量:4

Progress on the mechanisms of antifibrotic effects of PPARγ
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摘要 外照射放射治疗是癌症的主要治疗方式,然而放疗后放射性肺纤维化比较常见。它不仅影响患者的生存质量并限制治疗,甚至可致命。转化生长因子(TGF-β)是纤维化重要的调控因素,它可刺激纤维母细胞分化为成纤维细胞,而成纤维细胞分化和激活及产生疤痕组织成分是肺纤维化的关键致病过程。过氧化物酶体增殖物激活受体(PPARs)为核激素受体超家族的配体活化转录因子。PPAR γ是纤维母细胞细胞分化的关键调节因素。许多报道显示内源和外源的PPARγ配体通过干扰TGF-β信号通路等多种机制来抑制纤维化,它们的抗纤维化作用涉及到PPARγ依赖和非PPARγ依赖两种机制。PPARγ激动剂有着潜在的放射性纤维化的治疗价值。 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.
出处 《实用肿瘤学杂志》 CAS 2015年第1期73-77,共5页 Practical Oncology Journal
关键词 放射性肺纤维化 成纤维细胞 转化生长因子 过氧化物酶体增殖物激活受体 Radiation induced pulmonary fibrosis Myofibroblast Transforming growth factor γ Peroxi-some proliferator activated receptor
作者简介 孙宇楠,女,(1988-),硕士研究生,从事放射治疗及放射损伤防护的研究 吴荣,E-mail:wur@sj-hospital.org
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