Macrophages and renal fibrosis

Area of Science:

• Nephrology
• Immunology
• Pathology

Background:

• Renal fibrosis is a critical factor in progressive kidney disease, regardless of the initial cause.
• It represents a final common pathway determining the ultimate outcome of renal damage.
• The fibrotic process involves numerous cellular and molecular mediators.

Purpose of the Study:

• To review the key cellular and molecular players in the fibrotic response of the injured kidney.
• To discuss the specific role of monocytes and macrophages in renal scarring.
• To highlight the impact of monocyte and macrophage phenotypes on renal fibrosis.

Main Methods:

• Review of experimental and human renal disease studies.
• Analysis of recent research on circulating monocytes and tissue macrophages.
• Synthesis of information on cellular and molecular mediators of fibrosis.

Main Results:

• Macrophages are consistently involved in renal fibrosis across diverse disease processes.
• Monocytes and macrophages exhibit multifaceted phenotypes that influence their in vivo role.
• Key players include leukocytes, myofibroblasts, cytokines, growth factors, metalloproteinases, and inhibitors.

Conclusions:

• Macrophages are central to the development of renal scarring.
• Understanding monocyte and macrophage heterogeneity is crucial for comprehending their role in fibrosis.
• Targeting these cells may offer therapeutic strategies for mitigating renal fibrosis.