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a(CHEBI:"carbon monoxide") -| bp(GOBP:"blood coagulation")
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Approximately 61,000 statements.
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It has been shown that exogenous CO (ca. 300 parts per million) reduces inflammatory responses in several models of oxidant injury, which is consistent with results observed with HO-1 overexpression (Abraham et al., 1995a; Amersi et al., 1999). Although CO acts in many ways that are similar to NO, CO possesses additional functions on signal transduction pathways. CO inhibits pro-inflammatory genes while augmenting antiinflammatory cytokine production by selective activation of several p38 mitogen-activated protein kinase (MAPK) signaling pathways in a guanylyl cyclase-independent manner (Brouard et al., 2000; Otterbein et al., 2000; Sarady et al., 2002; Song et al., 2003). Other important effects of CO involve inhibition of proliferation of vascular smooth muscle cells, inhibition of platelet aggregation, protection against apoptosis, and acting as a neurotransmitter (Brune and Ullrich, 1987; Durante and Schafer, 1998; Brouard et al., 2000; Togane et al., 2000; Baranano and Snyder, 2001). Therefore, although high amounts of CO are lethal, low concentrations of CO mediate many important physiological functions, such as maintenance of vasomotor tone and mediating neurotransmission (Johnson et al., 1999).
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