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10.1152/ajplung.00221.2016 http://scihub22266oqcxt.onion/10.1152/ajplung.00221.2016 27474089!5142210!27474089     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27474089&cmd=llinks): Failed to open stream: HTTP request failed! 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Influences of innate immunity, autophagy, and fibroblast activation in the pathogenesis of lung fibrosis |pdf=|usr=}}{{27474089}} gab.com Text Influences of innate immunity, autophagy, and fibroblast activation in the pathogenesis of lung fibrosis JO: Am J Physiol Lung Cell Mol Physiol http://www.kidney.de/pget.php?&tw=1&pmid=27474089 #FOAvip Idiopathic pulmonary fibrosis (IPF) is a progressive interstitial lung disease characterized by accumulation of extracellular matrix (ECM) and impaired gas exchange. The pathobiological mechanisms that account for disease progression are poorly understood but likely involve alterations in innate inflammatory cells, epithelial cells, and fibroblasts. Thus we seek to review the most recent literature highlighting the complex roles of neutrophils and macrophages as both promoters of fibrosis and defenders against infection. With respect to epithelial cells and fibroblasts, we review the data suggesting that defective autophagy promotes the fibrogenic potential of both cell types and discuss new evidence related to matrix metalloproteinases, growth factors, and cellular metabolism in the form of lactic acid generation that may have consequences for promoting fibrogenesis. We discuss potential cross talk between innate and structural cell types and also highlight literature that may help explain the limitations of current IPF therapies. Twit Text FOAVip Influences of innate immunity, autophagy, and fibroblast activation in the pathogenesis of lung fibrosis ????Am J Physiol Lung Cell Mol Physiol http://www.kidney.de/pget.php?&tw=1&pmid=27474089 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27474089 #FOAvip English Wikipedia <ref>{{Cite pmid|27474089}}</ref> Influences of innate immunity, autophagy, and fibroblast activation in the pathogenesis of lung fibrosis #MMPMID27474089 O'Dwyer DN; Ashley SL; Moore BB Am J Physiol Lung Cell Mol Physiol 2016[Sep]; 311 (3): L590-601 PMID27474089show ga Idiopathic pulmonary fibrosis (IPF) is a progressive interstitial lung disease characterized by accumulation of extracellular matrix (ECM) and impaired gas exchange. The pathobiological mechanisms that account for disease progression are poorly understood but likely involve alterations in innate inflammatory cells, epithelial cells, and fibroblasts. Thus we seek to review the most recent literature highlighting the complex roles of neutrophils and macrophages as both promoters of fibrosis and defenders against infection. With respect to epithelial cells and fibroblasts, we review the data suggesting that defective autophagy promotes the fibrogenic potential of both cell types and discuss new evidence related to matrix metalloproteinases, growth factors, and cellular metabolism in the form of lactic acid generation that may have consequences for promoting fibrogenesis. We discuss potential cross talk between innate and structural cell types and also highlight literature that may help explain the limitations of current IPF therapies. |*Autophagy[MESH] |*Immunity, Innate[MESH] |Animals[MESH] |Fibroblasts/*physiology[MESH] |Humans[MESH] |Idiopathic Pulmonary Fibrosis/*immunology/metabolism/pathology[MESH] |Intercellular Signaling Peptides and Proteins/physiology[MESH] |Lactic Acid/metabolism[MESH] |Lung/immunology/metabolism/pathology[MESH]Influences of innate immunity, autophagy, and fibroblast activation in(epmc).pdf DeepDyve Pubget Overpricing