Several groups of researchers investigating the mechanisms of cell death have reported a puzzling result. Mice lacking the gene for Cyclophilin D appear to develop normally and additionally to be more resistant to cell necrosis.
Cells die in two ways. Apotosis is a controlled process in which the cell's contents are broken down before the cell membrane ruptures thereby avoiding inflammatory damage to nearby tissue. Necrosis is an uncontrolled process which occurs in response to injury such as lack of oxygen and causes further injury to nearby tissue.
When blood supply to a tissue is disrupted (ischaemia), cells begin to die by necrosis. If a long time elapses before blood flow is restored (reperfusion), additional cells undergo necrosis causing even further damage to the tissue. The recent research establishes that Cyclophilin D mediates the process of necrosis after reperfusion.
The puzzling finding is that mice lacking Cyclophilin D develop normally but also appear to be protected from reperfusion injury following ischaemia. Why would a gene that appears to confer no benefit and actually exacerbate injury be conserved in the mouse genome?
Ref: Nature 31-Mar-2005 Pg 658
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