Fibrosis of two: Epithelial cell-fibroblast interactions in pulmonary fibrosis.
Fibrosis of two: Epithelial cell-fibroblast interactions in pulmonary fibrosis.
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DOI：
10.1016/j.bbadis.2013.03.001
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发表时间：
2013-07
影响因子：
6.2
通讯作者：
Tager, Andrew M.
中科院分区：
文献类型：
--
作者：
Sakai, Norihiko;Tager, Andrew M.
特发性肺纤维化（IPF）的特征在于肺中成纤维细胞和细胞外基质的进行性和最终致命的积累，其扭曲其结构并损害其功能。IPF现在被认为是由伤口愈合过程引起的，尽管伤口愈合过程的启动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，导致病理性纤维化。虽然触发IPF的环境刺激仍有待确定，但最近的证据表明，它们最初损伤肺泡上皮。上皮损伤的重复循环和导致的肺泡上皮细胞死亡引起成纤维细胞的迁移、增殖、活化和肌成纤维细胞分化，导致这些细胞及其合成的细胞外基质的积累。反过来，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。虽然其他细胞类型肯定也有重要贡献，但我们在此关注的是“pas de deux”（两个步骤），或者可能更适合IPF的发病机制，即上皮细胞和成纤维细胞的“folie à deux”（两个疯狂），它推动了肺纤维化的进展。我们描述了介导这些细胞类型在其“两个纤维化”中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、音刺猬因子、前列腺素E2、血管紧张素II和活性氧。
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.
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影响因子：
4.9
作者：
Castelino FV;Varga J
通讯作者：
Varga J
影响因子：
8
作者：
Altenhofer, Sebastian;Kleikers, Pamela W. M.;Radermacher, Kim A.;Scheurer, Peter;Hermans, J. J. Rob;Schiffers, Paul;Ho, Heidi;Wingler, Kirstin;Schmidt, Harald H. H. W.
通讯作者：
Schmidt, Harald H. H. W.
DOI：
10.1152/ajplung.00530.2007
发表时间：
2008-10-01
影响因子：
4.9
作者：
Bogatkevich, Galina S.;Ludwicka-Bradley, Anna;Silver, Richard M.
通讯作者：
Silver, Richard M.
影响因子：
9.3
作者：
Caraci, Filippo;Gili, Elisa;Vancheri, Carlo
通讯作者：
Vancheri, Carlo
DOI：
10.1164/ajrccm/144.5.1080
发表时间：
1991-11-01
期刊：
AMERICAN REVIEW OF RESPIRATORY DISEASE
影响因子：
--
作者：
BOROK, Z;GILLISSEN, A;CRYSTAL, RG
通讯作者：
CRYSTAL, RG