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10.1007/s00109-021-02113-y http://scihub22266oqcxt.onion/10.1007/s00109-021-02113-y 34258628!8277227!34258628     free     free     free Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Mol+Med+(Berl) 2021 ; 99 (10): 1373-1384 Nephropedia Template TP {{tp|p=34258628|t=2021. The interplay of DAMPs, TLR4, and proinflammatory cytokines in pulmonary fibrosis |pdf=|usr=}}{{34258628}} gab.com Text The interplay of DAMPs, TLR4, and proinflammatory cytokines in pulmonary fibrosis JO: J Mol Med (Berl) http://www.kidney.de/pget.php?&tw=1&pmid=34258628 #FOAvip Pulmonary fibrosis is a chronic debilitating condition characterized by progressive deposition of connective tissue, leading to a steady restriction of lung elasticity, a decline in lung function, and a median survival of 4.5 years. The leading causes of pulmonary fibrosis are inhalation of foreign particles (such as silicosis and pneumoconiosis), infections (such as post COVID-19), autoimmune diseases (such as systemic autoimmune diseases of the connective tissue), and idiopathic pulmonary fibrosis. The therapeutics currently available for pulmonary fibrosis only modestly slow the progression of the disease. This review is centered on the interplay of damage-associated molecular pattern (DAMP) molecules, Toll-like receptor 4 (TLR4), and inflammatory cytokines (such as TNF-alpha, IL-1beta, and IL-17) as they contribute to the pathogenesis of pulmonary fibrosis, and the possible avenues to develop effective therapeutics that disrupt this interplay. Twit Text FOAVip The interplay of DAMPs, TLR4, and proinflammatory cytokines in pulmonary fibrosis ????J Mol Med (Berl) http://www.kidney.de/pget.php?&tw=1&pmid=34258628 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34258628 #FOAvip English Wikipedia <ref>{{Cite pmid|34258628}}</ref> The interplay of DAMPs, TLR4, and proinflammatory cytokines in pulmonary fibrosis #MMPMID34258628 Bolourani S; Brenner M; Wang P J Mol Med (Berl) 2021[Oct]; 99 (10): 1373-1384 PMID34258628show ga Pulmonary fibrosis is a chronic debilitating condition characterized by progressive deposition of connective tissue, leading to a steady restriction of lung elasticity, a decline in lung function, and a median survival of 4.5 years. The leading causes of pulmonary fibrosis are inhalation of foreign particles (such as silicosis and pneumoconiosis), infections (such as post COVID-19), autoimmune diseases (such as systemic autoimmune diseases of the connective tissue), and idiopathic pulmonary fibrosis. The therapeutics currently available for pulmonary fibrosis only modestly slow the progression of the disease. This review is centered on the interplay of damage-associated molecular pattern (DAMP) molecules, Toll-like receptor 4 (TLR4), and inflammatory cytokines (such as TNF-alpha, IL-1beta, and IL-17) as they contribute to the pathogenesis of pulmonary fibrosis, and the possible avenues to develop effective therapeutics that disrupt this interplay. |Alarmins/*metabolism[MESH] |Animals[MESH] |Cytokines/*metabolism[MESH] |Humans[MESH] |Idiopathic Pulmonary Fibrosis/complications/*metabolism/therapy[MESH] |Inflammation/complications/*metabolism[MESH] |Models, Biological[MESH]The interplay of DAMPs, TLR4, and proinflammatory cytokines in pulmona(epmc).pdf DeepDyve Pubget Overpricing