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Published on: November 10, 2021
Inflammatory processes in renal fibrosis
Xiao-Ming Meng1, David J Nikolic-Paterson2, Hui Yao Lan3
1School of Pharmacy, Anhui Medical University, 81 Meishan Road, Hefei, Anhui 230032, China.
Abstract:
Many types of kidney injury induce inflammation as a protective response. However, unresolved inflammation promotes progressive renal fibrosis, which can culminate in end-stage renal disease. Kidney inflammation involves cells of the immune system as well as activation of intrinsic renal cells, with the consequent production and release of profibrotic cytokines and growth factors that drive the fibrotic process. In glomerular diseases, the development of glomerular inflammation precedes interstitial fibrosis; although the mechanisms linking these events are poorly understood, an important role for tubular epithelial cells in mediating this link is gaining support. Data have implicated macrophages in promoting both glomerular and interstitial fibrosis, whereas limited evidence suggests that CD4(+) T cells and mast cells are involved in interstitial fibrosis. However, macrophages can also promote renal repair when the cause of renal injury can be resolved, highlighting their plasticity. Understanding the mechanisms by which inflammation drives renal fibrosis is necessary to facilitate the development of therapeutics to halt the progression of chronic kidney disease.
Insights
Unresolved kidney inflammation drives progressive renal fibrosis and end-stage renal disease. Understanding immune cell roles in this process is key to developing new therapies for chronic kidney disease.
Area of Science:
- Nephrology
- Immunology
- Pathology
Background:
- Kidney injury often triggers inflammation as a defense mechanism.
- Persistent inflammation, however, accelerates renal fibrosis, potentially leading to end-stage renal disease.
- The interplay between inflammation and fibrosis in kidney disease is complex, involving immune and intrinsic renal cells.
Purpose of the Study:
- To elucidate the mechanisms by which inflammation drives renal fibrosis.
- To identify key cellular players and molecular mediators in the inflammation-fibrosis axis.
- To provide a foundation for developing targeted therapeutics for chronic kidney disease.
Main Methods:
- Review and synthesis of existing data on kidney inflammation and fibrosis.
- Analysis of the roles of various immune cells (macrophages, T cells, mast cells) and intrinsic renal cells.
- Examination of profibrotic cytokine and growth factor production.
Main Results:
- Inflammation, if unresolved, promotes progressive renal fibrosis.
- Tubular epithelial cells are increasingly recognized for their role in linking glomerular inflammation to interstitial fibrosis.
- Macrophages are implicated in both promoting fibrosis and facilitating repair, demonstrating plasticity.
Conclusions:
- Understanding the mechanisms linking inflammation to renal fibrosis is crucial.
- Targeting these mechanisms may halt the progression of chronic kidney disease.
- Further research into immune cell plasticity and cellular crosstalk is warranted.
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