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首页> 外文期刊>Biochimica et biophysica acta. Molecular basis of disease: BBA >Fibrosis of two: Epithelial cell-fibroblast interactions in pulmonary fibrosis
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Fibrosis of two: Epithelial cell-fibroblast interactions in pulmonary fibrosis

机译：纤维化之二：肺纤维化中的上皮细胞-成纤维细胞相互作用

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Idiopathic pulmonary fibrosis (IPF) is characterized by the progressive and ultimately fatal accumulation of fibroblasts and extracellular matrix in the lung that distorts its architecture and compromises its function. IPF is now thought to result from wound-healing processes that, although initiated to protect the host from injurious environmental stimuli, lead to pathological fibrosis due to these processes becoming aberrant or over-exuberant. Although the environmental stimuli that trigger IPF remain to be identified, recent evidence suggests that they initially injure the alveolar epithelium. Repetitive cycles of epithelial injury and resultant alveolar epithelial cell death provoke the migration, proliferation, activation and myofibroblast differentiation of fibroblasts, causing the accumulation of these cells and the extracellular matrix that they synthesize. In turn, these activated fibroblasts induce further alveolar epithelial cell injury and death, thereby creating a vicious cycle of pro-fibrotic epithelial cell-fibroblast interactions. Though other cell types certainly make important contributions, we focus here on the "pas de deux" (steps of two), or perhaps more appropriate to IPF pathogenesis, the "folie à deux" (madness of two) of epithelial cells and fibroblasts that drives the progression of pulmonary fibrosis. We describe the signaling molecules that mediate the interactions of these cell types in their "fibrosis of two", including transforming growth factor-β, connective tissue growth factor, sonic hedgehog, prostaglandin E2, angiotensin II and reactive oxygen species. This article is part of a Special Issue entitled: Fibrosis: Translation of basic research to human disease.
机译：特发性肺纤维化（IPF）的特征是肺中成纤维细胞和细胞外基质的进行性和最终致命性积累，这会扭曲其结构并损害其功能。现在认为IPF是由伤口愈合过程导致的，尽管伤口愈合过程开始是为了保护宿主免受有害的环境刺激，但由于这些过程变得异常或过度旺盛而导致病理性纤维化。尽管触发IPF的环境刺激物尚待确定，但最近的证据表明，它们最初会损伤肺泡上皮。上皮损伤的重复循环和由此产生的肺泡上皮细胞死亡，引起成纤维细胞的迁移，增殖，活化和成纤维细胞分化，从而导致这些细胞及其合成的细胞外基质的积累。继而，这些活化的成纤维细胞诱导进一步的肺泡上皮细胞损伤和死亡，从而产生促纤维化上皮细胞-成纤维细胞相互作用的恶性循环。尽管其他类型的细胞当然也做出了重要的贡献，但我们还是将重点放在“双峰”（两个步骤）上，或更适合IPF发病机理的上皮细胞和成纤维细胞的“卵双峰”（两个）上。驱动肺纤维化的发展。我们描述了在“两种纤维化”中介导这些细胞类型相互作用的信号分子，包括转化生长因子-β，结缔组织生长因子，声波刺猬，前列腺素E2，血管紧张素II和活性氧。本文是名为“纤维化：基础研究对人类疾病的翻译”的特刊的一部分。

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