An alarmin(g) consequence of stroke
Patients surviving a stroke are at an increased risk for subsequent cardiovascular events. Preclinical models have shown accelerated atherosclerosis after stroke; however, the mechanisms underlying this enhanced plaque formation and inflammation in arteries have not been investigated. Now, Roth et al. have discovered that stroke-induced alarmin high-mobility group box 1 (HMGB1) release and sympathetic stress response activation exert a synergistic effect, resulting in exacerbation of atherosclerotic plaques in mice. The authors suggest that interfering with these processes after stroke might reduce the risk of secondary cardiovascular events.
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