Abstract
In 2016, an estimated 486,000 individuals sustained burn injuries requiring medical attention. Severe burn injuries lead to a persistent, hyperinflammatory response that may last up to 2 years. The persistent release of inflammatory mediators contributes to end-organ dysfunction and changes in genome expression. Burn-induced cardiac dysfunction may lead to heart failure and changes in cardiac remodeling. Cytokines promote the inflammatory cascade and promulgate mechanisms resulting in cardiac dysfunction. Here, we review the mechanisms by which TNFα, IL-1 beta, IL-6, and IL-10 cause cardiac dysfunction in post-burn injuries. We additionally review changes in the cytokine transcriptome caused by inflammation and burn injuries.