Abstract
Cardiovascular disease (CVD) remains a leading cause of mortality worldwide, with myocardial infarction (MI) being a major contributor, particularly among individuals with obesity, a prevalent risk factor. Inflammation plays a key role in both MI and obesity, as well as in ischemia-reperfusion injury (I/R), the paradoxical cardiac injury response triggered by reperfusion. The complex cellular and molecular interplay between these risk factors in the context of MI remains incompletely understood. Preclinical research using murine models is crucial for studying disease mechanisms, identifying therapeutic targets, and advancing drug development. Despite promising preclinical findings, clinical translation of therapies targeting inflammation has been largely disappointing. A major shortcoming is the predominant use of healthy mice without comorbidities in studies of inflammation in MI. A deeper understanding of inflammatory signaling in mouse models of obesity and related metabolic disorders may help bridge the gap between preclinical research and successful clinical application. In this review, we focus on the specific role of inflammation in MI murine models with obesity and related metabolic disorders. We aim to provide a better understanding of the apparent variability in their cardiac injury phenotype, address the existing controversies in reported data, and highlight directions for future research.