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Updated: Jan 30, 2026
Isolation, Characterization, and Purification of Macrophages from Tissues Affected by Obesity-related Inflammation
Published on: April 3, 2017
Macrophages: versatile players in renal inflammation and fibrosis
Patrick Ming-Kuen Tang1,2, David J Nikolic-Paterson3, Hui-Yao Lan4
1Department of Medicine & Therapeutics, Li Ka Shing Institute of Health Sciences, and Lui Che Woo Institute of Innovative Medicine, The Chinese University of Hong Kong, Shatin, Hong Kong, China.
Abstract:
Macrophages have important roles in immune surveillance and in the maintenance of kidney homeostasis; their response to renal injury varies enormously depending on the nature and duration of the insult. Macrophages can adopt a variety of phenotypes: at one extreme, M1 pro-inflammatory cells contribute to infection clearance but can also promote renal injury; at the other extreme, M2 anti-inflammatory cells have a reparative phenotype and can contribute to the resolution phase of the response to injury. In addition, bone marrow monocytes can differentiate into myeloid-derived suppressor cells that can regulate T cell immunity in the kidney. However, macrophages can also promote renal fibrosis, a major driver of progression to end-stage renal disease, and the CD206+ subset of M2 macrophages is strongly associated with renal fibrosis in both human and experimental diseases. Myofibroblasts are important contributors to renal fibrosis and recent studies provide evidence that macrophages recruited from the bone marrow can transition directly into myofibroblasts within the injured kidney. This process is termed macrophage-to-myofibroblast transition (MMT) and is driven by transforming growth factor-β1 (TGFβ1)-Smad3 signalling via a Src-centric regulatory network. MMT may serve as a key checkpoint for the progression of chronic inflammation into pathogenic fibrosis.
Insights
Macrophages can transform into myofibroblasts, driving kidney fibrosis. This macrophage-to-myofibroblast transition (MMT) is a key factor in chronic kidney disease progression.
Area of Science:
- Nephrology
- Immunology
- Cell Biology
Background:
- Macrophages play crucial roles in kidney immune surveillance and homeostasis.
- Macrophage responses to kidney injury are diverse, ranging from pro-inflammatory (M1) to reparative (M2) phenotypes.
- Certain macrophage subsets, like CD206+ M2 cells, are linked to kidney fibrosis, a major cause of end-stage renal disease.
Purpose of the Study:
- To investigate the direct transition of bone marrow-derived macrophages into myofibroblasts within the injured kidney.
- To elucidate the molecular mechanisms driving this macrophage-to-myofibroblast transition (MMT).
- To understand the role of MMT as a checkpoint in the progression of kidney inflammation to fibrosis.
Main Methods:
- Utilized experimental models of kidney injury.
- Investigated cellular differentiation pathways of macrophages.
- Analyzed molecular signaling pathways, including TGFβ1-Smad3 and Src-centric networks.
Main Results:
- Demonstrated that recruited bone marrow monocytes can differentiate directly into myofibroblasts in the injured kidney.
- Identified transforming growth factor-β1 (TGFβ1)-Smad3 signaling as a key driver of MMT.
- Highlighted a Src-centric regulatory network involved in the MMT process.
Conclusions:
- Macrophage-to-myofibroblast transition (MMT) is a significant pathway contributing to kidney fibrosis.
- MMT represents a critical checkpoint linking chronic kidney inflammation to pathogenic fibrosis.
- Targeting MMT may offer a therapeutic strategy for mitigating kidney fibrosis progression.
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