Signaling pathways involved in proteinase-activated receptor1-induced proinflammatory and profibrotic mediator release following lung injury.
The proteinase-activated receptors (PAR1 to 4) represent important novel therapeutic targets in fibroproliferative lung disorders, linking signals from coagulation proteinases to the production of proinflammatory and profibrotic mediators, in response to lung injury. This review focuses on the current understanding of cytokine and chemokine release downstream of PAR1 activation in the context of fibroproliferative lung disease, with an emphasis on the induction of the chemokine CCL2/MCP-1.
Mercer
Paul F
PF
Centre for Respiratory Research, University College London, 5 University Street, WC1E 6JJ London, UK. Paul.Mercer@ucl.ac.uk
Deng
Xiaoling
X
Chambers
Rachel C
RC
D000818:Animals; D018932:Chemokine CCL2 / Q000378:metabolism; D018925:Chemokines / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D005355:Fibrosis; D007249:Inflammation; D018836:Inflammation Mediators / Q000378:metabolism*; D008168:Lung / Q000473:pathology*; D055370:Lung Injury; D051379:Mice; D008954:Models, Biological; D010455:Peptides / Q000737:chemistry; D044463:Receptor, PAR-1 / Q000378:metabolism*; D015398:Signal Transduction; D013917:Thrombin / Q000378:metabolism
D018932:Chemokine CCL2; D018925:Chemokines; D016207:Cytokines; D018836:Inflammation Mediators; D010455:Peptides; D044463:Receptor, PAR-1; D013917:Thrombin