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Updated: May 22, 2026
Renal Ischaemia Reperfusion Injury: A Mouse Model of Injury and Regeneration
Published on: June 7, 2014
The role played by perivascular cells in kidney interstitial injury
Andres Rojas1, Fan-Chi Chang, Shuei-Liong Lin
1Renal Division & Center for Lung Biology, Department of Medicine, and Institute of Stem Cell & Regenerative Medicine, University of Washington, Seattle, WA, USA.
Abstract:
Fibrosis of the kidney is a disease affecting millions worldwide and is a harbinger of progressive loss of organ function resulting in organ failure. Recent findings suggest that understanding mechanisms of development and progression of fibrosis will lead to new therapies urgently required to counteract loss of organ function. Recently, little-known cells that line the kidney microvasculature, known as pericytes, were identified as the precursor cells which become the scar-forming myofibroblasts. Kidney pericytes are extensively branched cells located in the wall of capillaries, embedded within the microvascular basement membrane, and incompletely envelope endothelial cells with which they establish focal contacts. In response to kidney injuries, pericytes detach from endothelial cells and migrate into the interstitial space where they undergo a transition into myofibroblasts. Detachment leads to fibrosis but also leaves an unstable endothelium, prone to rarefaction. Endothelial-pericyte crosstalk at the vascular endothelial growth factor receptors and platelet derived growth factor receptors in response to injury have been identified as major new targets for therapeutic intervention.
Insights
Kidney fibrosis, a major cause of organ failure, is driven by pericytes transforming into scar-forming cells. Targeting endothelial-pericyte communication offers new therapeutic avenues for kidney disease.
Area of Science:
- Nephrology
- Cell Biology
- Vascular Biology
Background:
- Kidney fibrosis is a significant global health issue, leading to progressive organ dysfunction and failure.
- Understanding the mechanisms driving fibrosis is crucial for developing effective treatments.
- Pericytes, cells in kidney microvasculature, are newly identified as key precursors to myofibroblasts responsible for scarring.
Purpose of the Study:
- To elucidate the role of pericytes in kidney fibrosis development.
- To identify key molecular interactions in kidney injury response.
- To explore potential therapeutic targets for combating kidney fibrosis.
Main Methods:
- The study focuses on the cellular and molecular mechanisms of kidney pericyte activation and transformation.
- Investigated the process of pericyte detachment from endothelial cells and migration.
- Examined the crosstalk between endothelial cells and pericytes via specific growth factor receptors.
Main Results:
- Kidney pericytes are identified as the primary source of myofibroblasts in fibrotic kidneys.
- Pericyte detachment from microvasculature initiates fibrosis and endothelial instability.
- Endothelial-pericyte crosstalk, particularly involving vascular endothelial growth factor and platelet derived growth factor receptors, is implicated in injury response.
Conclusions:
- Pericyte transformation into myofibroblasts is a central mechanism in kidney fibrosis.
- Disruption of the endothelial-pericyte relationship contributes to kidney damage.
- Targeting endothelial-pericyte signaling pathways presents a promising strategy for treating kidney fibrosis.
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