Cardiovascular diseases claim millions of lives annually, with MI and strokes accounting for the majority of deaths. Survivors of MI suffer from irreversible heart damage, impacting their quality of life and increasing the risk of recurrent infarctions or further complications. The lack of effective therapies to restore heart function after MI highlights a critical unmet clinical need.

An effective immune response after MI is crucial for repairing cardiac damage and can coordinate pro-regenerative efforts from the other major cardiac cell types. Although the immune system is necessary for cardiac repair, prolonged inflammation exacerbates scarring, underscoring the importance of transient inflammation signals as a potential MI repair mechanism. The Tzahor lab discovered that a specific population of resident cardiac macrophages with a cardio-protective role express CCL24, a chemokine that induces angiogenesis and modulates the immune response. Direct administration of CCL24 peptide just after MI improves key functional cardiac parameters, reduces scar size, and facilitates angiogenesis (Figure 1), thereby enhancing cardiac repair after MI injury.