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Description
Because typical early atherosclerotic lesion formation observed in hyperhomocysteinemic animals can be prevented by an antiplatelet therapy with dipyridamole, the authors concluded that platelet-mediated proliferation of smooth muscle cells is a potential cellular mechanism involved in the atherogenicity of hyperhomocysteinemia
PMID: 7540457
Call Don D
Conversely, depletion of SCO2 instigates a metabolic shift toward glycolysis, mirroring observations in p53-deficient cells (Delavalle et al., 2011)
