Abstract
Inflammation is a key element in the early phase of reparative fibrosis following myocardial infarction (MI). Altering the onset, intensity, or duration of inflammation can dramatically impact the heart's structure and function. A weak inflammatory response may lead to fatal myocardial rupture due to excessive ECM degradation or impaired scar formation. An exaggerated or prolonged inflammatory response could cause excessive scar formation, resulting in increased LV stiffness. MAP kinase-activated protein kinase-2 (MK2), a protein serine/threonine kinase, is activated by p38 alpha and beta in response to cellular stress.
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