Vitamin C, collagen, and cracks in the plaque.

Most fatal acute myocardial infarctions result from a fracture of the plaque’s fibrous cap. We proposed the hypothesis some years ago that the level of collagen in the fibrous cap depends on a dynamic balance of synthesis and degradation.1 We further showed that inflammatory cytokines can regulate both the expression of genes that direct interstitial collagen synthesis in vascular smooth muscle cells and the interstitial collagenases (matrix metalloproteinases 1, 8, and 13) required to initiate the breakdown of collagen fibrils.2–5 Given the capital importance of collagen in protecting the plaque from rupture and hence thrombosis, the metabolism of this complex molecule merits consideration in depth.