id	author	title	date	pages	extension	mime	words	sentences	flesch	summary	cache	txt
cord-023867-ti4b03lh	Zuo, Wei	SARS Coronavirus and Lung Fibrosis	2009-07-22		.txt	text/plain	4277	244	51	The mechanisms by which SARS-CoV infection causes lung fibrosis are not fully understood, but transforming growth factor-β (TGF-β) and angiotensin-converting enzyme 2 (ACE2)-mediated lung fibrosis are among the most documented ones. Therefore, SARS-CoV infection may lead to lung fibrosis through multiple signaling pathways and TGF-β activation is one of the major contributors. ACE2 proteins are expressed by alveolar epithelial cells, the primary targets of SARS-CoV in lung. Altogether, infection with SARS-CoV results in ACE2 downregulation through the binding of SARS-CoV spike protein to ACE2, and this spike protein-mediated ACE2 downregulation is responsible for the pathogenesis of lung fibrosis by upregulating ANG-II and activating TGF-b signaling. Both the TGF-b/Smad and the ACE2/ANG-II/CTGF pathways contribute to myofibroblast activation and ECM accumulation, collectively leading to the final lung fibrosis Role of extracellular signal-regulated kinase, p38 kinase, and activator protein-1 in transforming growth factor-beta 1-induced alpha smooth muscle actin expression in human fetal lung fibroblasts in vitro Severe acute respiratory syndrome-associated coronavirus nucleocapsid protein interacts with Smad3 and modulates transforming growth factor-beta signaling	./cache/cord-023867-ti4b03lh.txt	./txt/cord-023867-ti4b03lh.txt