Interleukin-1β Blockade Improves Left Ventricular Systolic/Diastolic Function and Restores Contractility Reserve in Severe Ischemic Cardiomyopathy in the Mouse

Abstract

IL-1β blockade using a monoclonal antibody in mice with severe LV dysfunction after AMI prevents further deterioration in LV systolic and diastolic function and restores contractile reserve.

Pharmacologic Inhibition of the NLRP3 Inflammasome Preserves Cardiac Function After Ischemic and Nonischemic Injury in the Mouse

“…In this model, the benefit appears to be, at least in part, independent of infarct scar size and more directly related to attenuation of ischemic cardiomyopathy. 7 This is in agreement with the literature regarding the beneficial effects of IL-1β blockers in the mouse, 19–22 and preliminary data from pilot clinical trials. 6, 23, 24 …”

Pediatric and adult dilated cardiomyopathy represent distinct pathological entities

“…While the precise mechanisms that orchestrate proinflammatory responses in adult heart failure are not completely understood, it is clear that inhibition of inflammatory cytokine signaling may be beneficial (64). Blockade of IL1β signaling improves LV systolic function and suppresses components of adverse remodeling, including cardiomyocyte hypertrophy and myocardial fibrosis (65)(66)(67)(68)(69)(70). As such, IL1β antagonists are under clinical investigation as novel therapeutics for adults with acute myocardial infarction (MI) and heart failure (71,72).…”

Hesperetin protects against inflammatory response and cardiac fibrosis in postmyocardial infarction mice by inhibiting nuclear factor κB signaling pathway

“…An early study has found that application of reduced the degree of MI glucocorticoids in dogs due to their anti-inflammatory action, which proves that inflammation has a critical role in MI (3). Subsequent studies have found that macrophages, T lymphocytes, tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and IL-6 all have important roles in the area of MI and the deterioration of cardiac function after MI (4)(5)(6). Proinflammatory factors, including TNF-α, IL-1β and IL-6, are not continuously expressed in normal myocardial tissue, and the production or up-regulated expression of these factors represents an internal resistance to myocardial injury (1).…”