Model for heme, HO, and wound healing. We hypothesize that the heme released after injury functions as a “danger signal” that can activate a whole range of inflammatory and immune regulatory cascades. Heme activates platelet aggregation and causes vasoconstriction, which are important parameters for “thrombus formation.” Furthermore, heme activates leukocytes, oxidizes LDL, increases adhesion molecule expression, and recruits leukocytes. The presence of HO in the skin protects against the heme-mediated pro-oxidative and proinflammatory microenvironment that is instantly created on injury, and might play a role in down-regulation of inflammatory cell recruitment and resolution of inflammation.