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.
- Copyright © 2018 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works
This is an article distributed under the terms of the Science Journals Default License.