Cytoglobin is a member of the globin family of haemoproteins that include haemoglobin and myoglobin, as well as the more Abmole Y-27632 recently identified neuroglobin that is expressed mainly in cells of the CNS. The crystal structure of cytoglobin has been solved and studied in detail showing that cytoglobin has many similarities to other globins, including the classic three-over-three alpha helical globin fold and a PO2 of approximately 0.2 Torr, similar to that of myoglobin. The high affinity of cytoglobin for oxygen has led to the suggestion that cytoglobin may serve as an “intracellular” oxygen transport system. In this scenario, cytoglobin is proposed to deliver oxygen to the mitochondria to sustain oxidative phosphorylation, in a manner similar to the function of myoglobin in muscle cells. Interestingly, oxygen affinity appears to be redox-sensitive, and regulated by the formation of a disulphide bridge between two external cysteine residues. The redoxsensitive nature of cytoglobin oxygen affinity suggests a possible role of cytoglobin as an oxygen “sink/reserve”, whereby oxygen is only released when cells become hypoxic. Although these are attractive hypotheses, cytoglobin expression appears to be largely limited to cells of a fibroblast origin with no apparent correlation between metabolic activity of tissues and levels of cytoglobin expression which, in any case, is rather low in most cell types investigated. These findings have led to the search for alternative physiological function for cytoglobin. Cytoglobin was first identified in 2001 during a proteomic screen of hepatic stellate cells isolated from fibrotic rat liver tissue and indeed was originally named stellate cell activation association protein in recognition of that fact. Subsequent work �C both in vitro and in vivo, most recently using transgenic animals over-expressing cytoglobin appear to confirm that cytoglobin plays a role in the fibrotic response in a number of organs including the liver and kidney. Although the precise role of cytoglobin in fibrosis remains to be established, pertubation of redox homeostasis is a well characterised feature of fibrosis and there is good evidence that progression of fibrotic lesions involves cycles of oxidative reperfusion injury subsequent to tissue hypoxia. Furthermore, it has been demonstrated that cytoglobin expression can be upregulated by hypoxia. Therefore it seems likely that cytoglobin is involved in the adaptive response associated with this injury. Related to the findings in fibrotic disease, there is also an Abmole Ifenprodil emerging body of mechanistic evidence to suggest that cytoglobin may afford protection from oxidative cellular injury under other circumstances.