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Published on: November 10, 2021
Toll-like receptor activation: from renal inflammation to fibrosis
Wai Han Yiu1, Miao Lin1, Sydney C W Tang1
1Division of Nephrology, Department of Medicine, Queen Mary Hospital, The University of Hong Kong , Hong Kong.
Abstract:
Toll-like receptors (TLRs) are a conserved family of pattern recognition receptors that play a fundamental role in the innate immune system by triggering proinflammatory signaling pathways in response to microbial pathogens through exogenous pathogen-associated molecular patterns or tissue injury through endogenous danger-associated molecular patterns. In the kidney, TLRs are widely expressed in a variety of cell types. Emerging evidence demonstrates the participation of TLRs in the activation of these cells during renal fibrosis. This review highlights the role of TLRs and their endogenous ligands in the pathogenesis of renal fibrosis using ureteral obstruction and diabetic nephropathy as models of chronic kidney disease.
Insights
Toll-like receptors (TLRs) are crucial in the innate immune system and kidney disease. This review explores how TLRs and their ligands contribute to renal fibrosis in chronic kidney disease models.
Area of Science:
- Immunology
- Nephrology
- Cell Biology
Background:
- Toll-like receptors (TLRs) are key pattern recognition receptors in innate immunity.
- TLRs detect microbial and endogenous danger signals, initiating inflammatory responses.
- In the kidney, TLRs are expressed in diverse cell types and implicated in renal fibrosis.
Approach:
- This review synthesizes current evidence on the role of TLRs in renal fibrosis.
- It utilizes ureteral obstruction and diabetic nephropathy as models of chronic kidney disease.
- The focus is on the contribution of TLRs and their endogenous ligands to disease pathogenesis.
Key Points:
- TLRs are widely expressed in renal cells and play a role in fibrosis.
- Endogenous ligands of TLRs contribute to the inflammatory processes driving renal fibrosis.
- Specific TLR pathways are activated during chronic kidney disease progression.
Conclusions:
- TLRs and their endogenous ligands are significant contributors to renal fibrosis.
- Targeting TLR signaling presents a potential therapeutic strategy for chronic kidney diseases.
- Further research is needed to fully elucidate TLR involvement in kidney disease pathogenesis.
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