Key result
Activation of the inflammasome during myocardial injury promotes adverse cardiac remodeling, while pilot trials suggest that blocking inflammasome-derived IL-1β has beneficial effects on cardiac function.
The inflammasome is a key mediator of adverse cardiac remodeling following myocardial injury, representing a potential therapeutic target.
Highlights IL-1β blockade as a promising but unproven target for preventing post-injury heart.
SIGNIFICANCE: An inflammatory response follows an injury of any nature, and while such a response is an attempt to promote healing, it may, itself, result in further injury. RECENT ADVANCES: The inflammasome is a macromolecular structure recently recognized as a central mediator in the acute inflammatory response. The inflammasome senses the injury and it amplifies the response by leading to the release of powerful pro-inflammatory cytokines, interleukin-1β (IL-1β) and IL-18. CRITICAL ISSUES: The activation of the inflammasome in the heart during ischemic and nonischemic injury represents an exaggerated response to sterile injury and promotes adverse cardiac remodeling and failure. FUTURE DIRECTIONS: Pilot clinical trials have explored blockade of the inflammasome-derived IL-1β and have shown beneficial effects on cardiac function. Additional clinical studies testing this approach are warranted. Moreover, specific inflammasome inhibitors that are ready for clinical use are currently lacking.
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Toldo et al. (2014) conducted a review in Myocardial injury and cardiac remodeling. Inflammasome blockade / IL-1β blockade was evaluated. Activation of the inflammasome during myocardial injury promotes adverse cardiac remodeling, while pilot trials suggest that blocking inflammasome-derived IL-1β has beneficial effects on cardiac function.
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