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Updated: Feb 20, 2026

Unilateral Ureteral Obstruction Model for Investigating Kidney Interstitial Fibrosis
Published on: April 25, 2025
Mechanisms of Renal Fibrosis
1Division of Nephrology, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri 63110, USA;
Abstract:
Tubulointerstitial fibrosis is a chronic and progressive process affecting kidneys during aging and in chronic kidney disease (CKD), regardless of cause. CKD and renal fibrosis affect half of adults above age 70 and 10% of the world's population. Although no targeted therapy yet exists to slow renal fibrosis, a number of important recent advances have clarified the cellular and molecular mechanisms underlying the disease. In this review, I highlight these advances with a focus on cells and pathways that may be amenable to therapeutic targeting. I discuss pathologic changes regulating interstitial myofibroblast activation, including profibrotic and proinflammatory paracrine signals secreted by epithelial cells after either acute or chronic injury. I conclude by highlighting novel therapeutic targets and approaches with particular promise for development of new treatments for patients with fibrotic kidney disease.
Insights
Tubulointerstitial fibrosis, a common kidney condition, progresses with age and chronic kidney disease (CKD). Recent advances clarify cellular mechanisms, identifying potential therapeutic targets for fibrotic kidney disease treatments.
Area of Science:
- Nephrology
- Pathology
- Molecular Biology
Background:
- Tubulointerstitial fibrosis is a progressive kidney condition linked to aging and chronic kidney disease (CKD).
- CKD and renal fibrosis impact a significant portion of the global population, particularly older adults.
- Currently, no specific therapies exist to halt the progression of renal fibrosis.
Purpose of the Study:
- To review recent advances in understanding the cellular and molecular mechanisms of tubulointerstitial fibrosis.
- To identify potential therapeutic targets within these mechanisms for treating fibrotic kidney disease.
- To discuss novel therapeutic strategies for patients suffering from kidney fibrosis.
Main Methods:
- Literature review focusing on cellular and molecular pathways in renal fibrosis.
- Analysis of pathological changes in interstitial myofibroblast activation.
- Examination of paracrine signaling between injured epithelial cells and surrounding tissues.
Main Results:
- Recent research has elucidated key cellular and molecular drivers of renal fibrosis.
- Profibrotic and proinflammatory signals from injured epithelial cells play a critical role.
- Interstitial myofibroblast activation is a central pathological process.
Conclusions:
- Novel therapeutic targets and approaches show promise for treating fibrotic kidney disease.
- Understanding cellular mechanisms offers new avenues for drug development.
- Targeting specific pathways could slow or reverse kidney fibrosis progression.
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