The majority of clinical studies demonstrate that patients with hyperhomocysteinaemia have an increased risk of atherothrombotic events. However, there is a striking and poorly understood heterogeneity in the severity of clinical features in individuals with hyperhomocysteinaemia. This observation suggests that other factors must exist that modulate the relationship between hyperhomocysteinaemia and clinical disease. Therefore identifying factors that inhibit or enhance the vasculotoxic effects of homocysteine is important, as is elucidation of how homocysteine damages blood vessels. This comment discusses the study of Woodman and colleagues in this issue of Clinical Science in which they investigate the effects of hyperhomocysteinaemia on endothelial function.

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