کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8260899 | 1534670 | 2013 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Fibrosis of two: Epithelial cell-fibroblast interactions in pulmonary fibrosis
ترجمه فارسی عنوان
فیبر دو: اثر متقابل سلول های اپیتلیال فیبروبلاست در فیبروز ریوی
دانلود مقاله + سفارش ترجمه
دانلود مقاله ISI انگلیسی
رایگان برای ایرانیان
کلمات کلیدی
PGE2TGF-βAECCTGFMyofibroblastsIPFROS - ROSHydrogen peroxide - آب اکسیژنهtransforming growth factor - تبدیل فاکتور رشدApoptosis - خزان یاختهایShh - خیرepithelial cells - سلول بافت پوششی یا اپیتلیومalveolar epithelial cell - سلول های اپیتلیال آلوئولارsonic hedgehog - صدای جیر جیرConnective tissue growth factor - فاکتور رشد بافت همبندFibroblasts - فیبروبلاست هاPulmonary fibrosis - فیبروز ریهidiopathic pulmonary fibrosis - فیبروز ریوی ایدیوپاتیکExtracellular matrix - ماتریکس خارج سلولیH2O2 - هیدروژن پراکسیدProstaglandin E2 - پروستاگلاندین E2Reactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
چکیده انگلیسی
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.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease - Volume 1832, Issue 7, July 2013, Pages 911-921
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease - Volume 1832, Issue 7, July 2013, Pages 911-921
نویسندگان
Norihiko Sakai,, Andrew M. Tager,