Background—Exaggerated and prolonged inflammation after myocardial infarction (MI)
accelerates left ventricular remodeling. Inflammatory pathways may present a therapeutic …

Myocardial infarction (MI) leads to a systemic surge of vascular inflammation in mice and
humans, resulting in secondary ischemic complications and high mortality. We show that, in …

Atherosclerotic lesional macrophages express molecules that promote plaque progression,
but lack of mechanisms to therapeutically target these molecules represents a major gap in …

Background Myocarditis is characterized by inflammatory cell infiltration of the heart and
subsequent deterioration of cardiac function. Monocytes are the most prominent population …

Aims Balance between inflammatory and reparative leucocytes allows optimal healing after
myocardial infarction (MI). Interindividual heterogeneity evokes variable functional outcome …

Background—Cell therapy with bone marrow–derived mononuclear cells (BMCs) can
improve recovery of cardiac function after ischemia; however, the molecular mechanisms …

Myocardial infarction triggers an inflammatory reaction that is involved in cardiac
remodeling. Cardiac repair is dependent on regulatory mechanisms that suppress …

Aims Acute myocardial infarction (MI) is the leading cause of mortality worldwide. Anti-
inflammatory strategies to reduce neutrophil-driven acute post-MI injury have been shown to …

Background After myocardial infarction (MI), inflammatory cells infiltrate the infarcted heart in
response to secreted stimuli. Monocytes are recruited to the infarct via CCR2 chemokine …

MicroRNA-based therapy that targets cardiac macrophages holds great potential for
treatment of myocardial infarction (MI). Here, we explored whether boosting the miRNA-21 …