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Cellular and molecular mechanisms of renal fibrosis
Open accessAbstract
Renal fibrosis, particularly tubulointerstitial fibrosis, is the common final outcome of almost all progressive chronic kidney diseases. Renal fibrosis is also a reliable predictor of prognosis and a major determinant of renal insufficiency. Irrespective of the initial causes, renal fibrogenesis is a dynamic and converging process that consists of four overlapping phases: priming, activation, execution and progression. Nonresolving inflammation after a sustained injury sets up the fibrogenic stage (priming) and triggers the activation and expansion of matrix-producing cells from multiple sources through diverse mechanisms, including activation of interstitial fibroblasts and pericytes, phenotypic conversion of tubular epithelial and endothelial cells and recruitment of circulating fibrocytes. Upon activation, matrix-producing cells assemble a multicomponent, integrin-associated protein complex that integrates input from various fibrogenic signals and orchestrates the production of matrix components and their extracellular assembly. Multiple cellular and molecular events, such as tubular atrophy, microvascular rarefaction and tissue hypoxia, promote scar formation and ensure a vicious progression to end-stage kidney failure. This Review outlines our current understanding of the cellular and molecular mechanisms of renal fibrosis, which could offer novel insights into the development of new therapeutic strategies.
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Rowe, R. G., Li, X.-Y., Hu, Y., Saunders, T. L., Virtanen, I., de Herreros, A. G., Becker, K.-F., Ingvarsen, S., Engelholm, L. H., Bommer, G. T., et al. (2009) · Journal of Cell Biology · doi:10.1083/jcb.200810113 · Cited by 161
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Stage-Specific Action of Matrix Metalloproteinases Influences Progressive Hereditary Kidney Disease
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Self-citationKang, Y. S., Li, Y., Dai, C., Kiss, L. P., Wu, C., & Liu, Y. (2010) · Kidney International · doi:10.1038/ki.2010.137 · Cited by 150
Self-citationPivotal role of CD4+ T cells in renal fibrosis following ureteric obstruction
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Self-citationRole of Mast Cells in Progressive Renal Diseases
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Early Epithelial Phenotypic Changes Predict Graft Fibrosis
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SnapShot: The Epithelial-Mesenchymal Transition
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Self-citationInhibition of Integrin-Linked Kinase Attenuates Renal Interstitial Fibrosis
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Essential role for Smad3 in angiotensin II‐induced tubular epithelial–mesenchymal transition
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Proteasomal Processing of Albumin by Renal Dendritic Cells Generates Antigenic Peptides
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By Homing to the Kidney, Activated Macrophages Potently Exacerbate Renal Injury
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Targeting the Recruitment of Monocytes and Macrophages in Renal Disease
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Mast Cell-Mediated Remodeling and Fibrinolytic Activity Protect against Fatal Glomerulonephritis
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Smooth Muscle α-Actin Deficiency in Myofibroblasts Leads to Enhanced Renal Tissue Fibrosis
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Novel actions of tissue-type plasminogen activator in chronic kidney disease
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Self-citationInvolvement of bone-marrow-derived cells in kidney fibrosis
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Opposite Action of Peroxisome Proliferator-activated Receptor-γ in Regulating Renal Inflammation
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Self-citationLoss of renal microvascular integrity in postnatal Crim1 hypomorphic transgenic mice
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Vitamin D in Chronic Kidney Disease: New Potential for Intervention
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tPA Is a Potent Mitogen for Renal Interstitial Fibroblasts
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Metadata
- Authors
- Liu, Y.
- Venue
- Nature Reviews Nephrology
- Published
- 2011-10-18
- Volume
- 7
- Issue
- 12
- Pages
- 684-696
- ISSN
- 1745-8323 (ISSN-L)
- 1759-5061
- 1759-507X
- OpenAlex
- W2033457930
- Cited by
- 1,446
- References
- 185
- FWCI
- 5.72
- Type
- journal article
- Language
- en
- Open access
- green
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