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Updated: May 22, 2026

Development of an In Vitro Assay to Evaluate Contractile Function of Mesenchymal Cells that Underwent Epithelial-Mesenchymal Transition
Published on: June 10, 2016
Epithelial-mesenchymal crosstalk alteration in kidney fibrosis
Marco Prunotto1, David C Budd, Giulio Gabbiani
1CV and Metabolic DTA Department, F. Hoffmann-La Roche Ltd, Basel, Switzerland. marco.prunotto@gmail.com
Abstract:
The incidence of chronic kidney diseases (CKD) is constantly rising, reaching epidemic proportions in the western world and leading to an enormous threat, even to modern health-care systems, in industrialized countries. Therapies of CKD have greatly improved following the introduction of drugs targeting the renin-angiotensin system (RAAS) but even this refined pharmacological approach has failed to stop progression to end-stage renal disease (ESRD) in many individuals. In vitro historical data and recent new findings have suggested that progression of renal fibrosis might occur as a result of an altered tubulo-interstitial microenvironment and, more specifically, as a result of an altered epithelial-mesenchymal crosstalk. Here we the review biological findings that support the hypothesis of an altered cellular crosstalk in an injured local tubulo-interstitial microenvironment leading to renal disease progression. Copyright © 2012 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
Insights
Chronic kidney disease (CKD) is rising globally. Altered cellular crosstalk in the tubulo-interstitial microenvironment may drive renal fibrosis and disease progression, despite improved therapies targeting the renin-angiotensin system (RAAS).
Area of Science:
- Nephrology
- Pathology
- Cell Biology
Background:
- Chronic kidney diseases (CKD) incidence is increasing globally, posing a significant public health challenge.
- Current therapies targeting the renin-angiotensin system (RAAS) have limitations in halting progression to end-stage renal disease (ESRD).
- Existing research suggests renal fibrosis progression is linked to the tubulo-interstitial microenvironment.
Purpose of the Study:
- To review biological evidence supporting the role of altered cellular crosstalk in CKD progression.
- To investigate the contribution of the tubulo-interstitial microenvironment to renal disease.
- To explore the epithelial-mesenchymal crosstalk in the context of renal fibrosis.
Main Methods:
- Literature review of in vitro and in vivo studies.
- Analysis of historical and recent findings on renal fibrosis mechanisms.
- Examination of cellular interactions within the tubulo-interstitial microenvironment.
Main Results:
- Evidence suggests that an altered tubulo-interstitial microenvironment contributes to CKD progression.
- Epithelial-mesenchymal crosstalk is identified as a key factor in the development of renal fibrosis.
- Cellular interactions within the injured kidney play a critical role in disease advancement.
Conclusions:
- Altered cellular crosstalk in the tubulo-interstitial microenvironment is a significant driver of renal fibrosis and CKD progression.
- Further research into these cellular mechanisms could reveal new therapeutic targets for CKD.
- Understanding epithelial-mesenchymal interactions is crucial for combating the epidemic of kidney disease.
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