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Published on: May 9, 2025
Macrophages in Renal Injury and Repair
Sarah C Huen1, Lloyd G Cantley1
1Section of Nephrology, Department of Internal Medicine, Yale University, New Haven, Connecticut 06520;
Abstract:
Acute kidney injury (AKI) is a growing global health concern, yet no treatment is currently available to prevent it or to promote kidney repair after injury. Animal models demonstrate that the macrophage is a major contributor to the inflammatory response to AKI. Emerging data from human biopsies also corroborate the presence of macrophages in AKI and their persistence in progressive chronic kidney disease. Macrophages are phagocytic innate immune cells that are important mediators of tissue homeostasis and host defense. In response to tissue injury, macrophages become activated based on specific signals from the damaged microenvironment. The activation and functional state of the macrophage depends on the stage of tissue injury and repair, reflecting a dynamic and diverse spectrum of macrophage phenotypes. In this review, we highlight our current understanding of the mechanisms by which macrophages contribute to injury and repair after AKI.
Insights
No treatments exist for acute kidney injury (AKI), a growing concern. This review explores how macrophages, key immune cells, contribute to kidney injury and repair processes.
Area of Science:
- Nephrology
- Immunology
- Cell Biology
Background:
- Acute kidney injury (AKI) is a significant global health issue with no current therapeutic interventions.
- Macrophages play a critical role in the inflammatory response to AKI, as evidenced in animal models and human biopsies.
- These innate immune cells are crucial for tissue homeostasis and host defense, exhibiting diverse phenotypes in response to injury.
Purpose of the Study:
- To review the current understanding of macrophage involvement in acute kidney injury.
- To elucidate the mechanisms by which macrophages contribute to kidney damage and subsequent repair.
- To highlight the dynamic nature of macrophage activation and function in the context of AKI.
Main Methods:
- Literature review of existing studies on macrophages in AKI.
- Analysis of data from animal models of kidney injury.
- Examination of human biopsy data correlating macrophage presence with AKI and chronic kidney disease.
Main Results:
- Macrophages are consistently identified as major contributors to inflammation in AKI.
- Macrophage presence is associated with progressive chronic kidney disease.
- Macrophage activation and phenotype are dynamic, influenced by the specific injury microenvironment.
Conclusions:
- Macrophages are central players in the pathogenesis and resolution of AKI.
- Understanding macrophage heterogeneity is crucial for developing AKI treatments.
- Targeting macrophage responses may offer a therapeutic strategy for preventing AKI or promoting kidney repair.
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