Immunity, Inflammation, and Oxidative Stress in Heart Failure: Emerging Molecular Targets

Abstract

Heart failure (HF) remains a major cause of morbidity and mortality worldwide. Although various therapies developed over the last two decades have shown improved long term outcomes in patients with established HF, there has been little progress in preventing the adverse cardiac remodeling that initiates HF. To fill the gap in treatment, current research efforts are focused on understanding novel mechanisms and signaling pathways. Immune activation, inflammation, oxidative stress, alterations in mitochondrial bioenergetics, and autophagy have been postulated as important pathophysiological events in this process. An improved understanding of these complex processes could facilitate a therapeutic shift toward molecular targets that can potentially alter the course of HF.