In the last decade inflammation has been recognized as playing an important role following ischemia-reperfusion injury and, as a consequence, to be an important therapeutic target for the treatment of heart failure. However, inflammation contributes differently to the pathogenesis of cardiac dysfunction and to different patterns of cardiac remodeling. Several mediators of inflammation trigger the remodeling cascade, a process that initially confers protection to the heart as a compensatory mechanism. Yet chronic inflammation after myocardial infarction also leads to cardiac remodeling that, when prolonged, leads to heart failure progression.

The diversity of inflammation further demonstrates the need for a tailored characterization of inflammation enabling subsequent target-specific strategies. This necessity is supported by the disappointing results to date of anti-inflammatory strategies used in heart failure patients.

This special issue is designed to focus on the interplay of inflammation and cell injury/death following myocardial ischemia-reperfusion. The issue also aims to investigate the impact of regulation of inflammatory signals on the evolution of cardiac remodeling and function and to identify novel potential therapeutic targets. Both basic science and clinical studies are welcomed.

Potential topics include but are not limited to the following:

• Characteristics and mechanisms of myocardial ischemia-reperfusion injury
• Mediators, pathways, and markers of inflammation in myocardial ischemia-reperfusion
• Cell injury and cell death and their role in inflammation following myocardial ischemia-reperfusion
• Kinetics of inflammatory response and repair in myocardial ischemia-reperfusion
• Oxidative stress and inflammation in myocardial ischemia-reperfusion
• Kinetics of interventions and their role in short and long-term remodeling
• Potential therapeutic targets to modulate inflammation following myocardial ischemia-reperfusion