Monocytes/macrophages are a heterogeneous cell population that play a critical role in host defense and tissue homeostasis. However, macrophage activation during acute and chronic inflammation can result in macrophage-mediated renal injury in a variety of settings, including proliferative glomerulonephritis. Macrophages can be activated via a number of intracellular signaling pathways (eg, c-Jun amino terminal kinase, p38 mitogen-activated protein kinase, FcR/Syk, Janus kinase/signal transducer and activator of transcription) that induce production of mediators of renal injury. Thus, targeting selected macrophage signaling pathways is a potential therapeutic strategy to suppress macrophage-mediated renal injury while leaving intact the desirable macrophage functions of host defense and tissue repair.
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