Development and Function of Arterial and Cardiac Macrophages

Abstract

Macrophages inhabit all major organs, and are capable of adapting their functions to meet the needs of their home tissues. The recent recognition that tissue macrophages derive from different sources, coupled with the notion that environmental cues and inflammatory stimuli can sculpt and agitate homeostasis, provides a frame of reference from which we can decipher the breadth and depth of macrophage activity. Here we discuss macrophages residing in the cardiovascular system, focusing particularly on their development and function in steady state and disease. Central to our discussion is the tension between macrophage ontogeny as a determinant of macrophage function, and the idea that tissues condition macrophage activities and supplant the influence of macrophage origins in favor of environmental demands.

Figure 1

Arterial and cardiac macrophages in disease and injury. During atherosclerosis or myocardial infarction, hematopoietic sites (bone marrow and to a lesser extent spleen) supply monocytes that infiltrate the aorta and ischemic myocardium, respectively. On influx, monocytes differentiate to macrophages, which can then proliferate. Both sites also contain populations of macrophages that have seeded the tissues during embryogenesis or just after birth. These tissue- derived macrophages self-renew through proliferation. Functions of tissue-derived vs. monocyte-derived macrophages in steady state and inflammation are discussed in text.