Cause or Consequence
Murray C.H. Clarke, Martin R. Bennett
Abstract
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Murray C.H. Clarke, Martin R. Bennett
Abstract
Open-access reader
C ell death is found in human and animal atherosclerotic plaques.[1][2][3][4] There is now extensive evidence for both apoptosis and necrosis, the latter being either a primary process or secondary to apoptosis (secondary necrosis).There is also extensive evidence that other processes or structural changes in the plaque accompany cell death, such as inflammation, thrombosis, calcification, and changes in size of both the fibrous cap and necrotic core (reviewed in 5 ).Plaque cell death is also associated with a systemic proinflammatory state, with changes in multiple serum cytokines.6 -8 However, the most difficult problem has been determining just what the cause and effect relationship is between cell death and these processes.Fortunately, studies performed over recent years have begun to directly address this problem.
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C ell death is found in human and animal atherosclerotic plaques.[1][2][3][4] There is now extensive evidence for both apoptosis and necrosis, the latter being either a primary process or secondary to apoptosis (secondary necrosis).There is also extensive evidence that other processes or structural changes in the plaque accompany cell death, such as inflammation, thrombosis, calcification, and changes in size of both the fibrous cap and necrotic core (reviewed in 5 ).Plaque cell death is also associated with a systemic proinflammatory state, with changes in multiple serum cytokines.6 -8 However, the most difficult problem has been determining just what the cause and effect relationship is between cell death and these processes.Fortunately, studies performed over recent years have begun to directly address this problem.
Key concepts: Apoptosis, Proinflammatory cytokine, Thrombosis, Fibrous cap, Programmed cell death, Necrosis, Medicine, Inflammation