Apoptosis in pulmonary fibrosis: Too much or not enough?
Apoptosis in pulmonary fibrosis: Too much or not enough?
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DOI：
10.1089/ars.2007.1907
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发表时间：
2008-02-01
影响因子：
6.6
通讯作者：
Fattman, Cheryl L.
中科院分区：
文献类型：
--
作者：
Fattman, Cheryl L.
细胞凋亡在正常肺稳态和与纤维化肺疾病相关的肺重塑中起重要作用。细胞凋亡是否促进或抑制肺纤维化的发病机制取决于所涉及的细胞类型和受影响的肺的微环境。肺泡上皮细胞的过度丢失可能在特发性肺纤维化（IPF）进展的早期很重要，而成纤维细胞和肌成纤维细胞凋亡减少与纤维化病变的形成有关。因此，基于刺激或抑制细胞凋亡的新型疗法可能证明对IPF患者的治疗有益。
Apoptosis plays an important role in both normal lung homeostasis and lung remodeling associated with fibrotic lung disease. Whether apoptosis promotes or inhibits the pathogenesis of pulmonary fibrosis depends upon the cell type involved and the microenvironment of the affected lung. Undue cell loss in the alveolar epithelium may be important early in idiopathic pulmonary fibrosis (IPF) progression, while reduced fibroblast and myofibroblast apoptosis has been associated with the formation of fibrotic lesions. As such, novel therapies based on the stimulation or inhibition of apoptosis may prove beneficial to the treatment of patients with IPF.