Key result
Post-ischemic trained immunity imprints progenitor inflammatory memory, driving persistent vascular inflammation and multimorbidity.
This review highlights trained immunity as a key mechanism linking acute ischemic events to long-term cardiovascular and metabolic multimorbidity, offering a framework for novel therapeutic interventions.
Despite major advances in acute reperfusion therapies, patients surviving ischemic stroke or myocardial infarction remain at high risk for long-term cardiovascular and metabolic comorbidities. Emerging evidence identifies trained immunity, the long-lasting reprogramming of innate immune progenitors, as a central driver of this interorgan communication. Sterile insults such as stroke or myocardial infarction imprint persistent inflammatory memory via long-lasting reprogramming of bone marrow hematopoietic progenitors, biasing myelopoiesis and generating proinflammatory monocytes that target distant organs. This central trained immunity explains how a single ischemic event can precipitate cardiac dysfunction, accelerate atherosclerosis, or exacerbate metabolic disease, thereby contributing to multimorbidity in vascular patients. Understanding these systemic immune circuits provides a conceptual framework for developing interventions that interrupt maladaptive inflammatory memory. Finally, we discuss emerging therapeutic strategies to prevent maladaptive innate immune memory and mitigate chronic vascular inflammation and multimorbidity.
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Arthur Liesz (2026) conducted a review in Ischemic stroke or myocardial infarction. Trained immunity was evaluated. Trained immunity following ischemic events imprints persistent inflammatory memory in bone marrow progenitors, driving chronic vascular inflammation and multimorbidity.
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