“…This is in line with other reports in which inhibition of the interaction of RAGE with its ligands led to a reduced inflammation in models of hepatic injury (19 -21), diabetic atherosclerosis (22, 23), delayed-type hypersensitivity (24, 25), type II collagen-induced arthritis (25), and sepsis (24). In addition, in a recent study, RAGE was found to be important for the development of lung fibrosis upon intratracheal administration of bleomycin (42). Because activation of RAGE triggers multiple intracellular signaling pathways, including NF-B, resulting in the transcription of proinflammatory factors (43,44), these findings could at least in part be attributed to the blockade of RAGE interaction with its ligands via diminished activation of NF-B, resulting in attenuated tissue injury/damage and/or inflammation (24,45).…”