Figure 3.

Cardiac macrophages in the context of stress conditions. Various stressors can activate macrophage subpopulations in heart (left). These stress conditions lead to an increase in macrophages by local proliferation and by recruitment of monocytes from bone marrow and spleen (right). Tissue-resident CCR2+ macrophages may further spur the recruitment of myeloid cells, remove tissue debris, and modulate the cardiac microenvironment by the release of matrix metalloproteinases (MMPs), proteases, and cytokines. The latter may exert beneficial or harmful effects—as illustrated for IL-10—depending on disease context and timing. DAMP, damage-associated molecular pattern.