ArticleAtherosclerosis2026
Inflammasome inhibition in myocardial infarction reduces early reperfusion injury and suppresses systemic plaque activation.
Article in Atherosclerosis, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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14 authors.
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Abstract
BACKGROUND AND
aimsActivation of innate immunity early after reperfused myocardial infarction (MI) contributes to reperfusion injury and acts systemically to accelerate atherosclerosis in remote non-culprit plaques. We hypothesized that inhibition of the NLRP3 inflammasome complex that is activated by damage-associated molecular patterns after MI would suppress these diverse maladaptive responses.
methodsIn hyperlipidemic Ldlr
resultsPost-MI treatment with MCC950 suppressed all three molecular imaging markers of microvascular reperfusion injury which was associated with a significant reduction in post-MI myocardial inflammatory cell infiltrate on day 3. Treatment with MCC950 resulted in a greater degree of recovery over time in all echocardiographic measures of LV function, and reduced histologic infarct size by 50% (p < 0.01). Mice undergoing MI had accelerated brachiocephalic plaque growth versus non-ischemic age-matched controls which was inhibited by MCC950 resulting in smaller plaque size and necrotic cores, larger smooth muscle cap thickness, and evidence for fibrous cap endothelial-mesenchymal transformation.
conclusionsIn reperfused MI, pharmacologic inhibition of the NLRP3 inflammasome suppresses inflammatory and thromboinflammatory processes that contribute to early reperfusion injury, infarct expansion, and remote non-culprit plaque activation in later phases.
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