Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

In-vitro Mutagenesis01:16

In-vitro Mutagenesis

To learn more about the function of a gene, researchers can observe what happens when the gene is inactivated or “knocked out,” by creating genetically engineered knockout animals. Knockout mice have been particularly useful as models for human diseases such as cancer, Parkinson’s disease, and diabetes.

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Prenatal body fluid analysis in the evaluation of CAKUT.

Pediatric nephrology (Berlin, Germany)·2026
Same author

Urinary Collagen Peptides Predict Mortality.

Proteomics·2026
Same author

In silico prediction of optimal multifactorial intervention in chronic kidney disease.

Journal of translational medicine·2025
Same author

Toxicity and therapeutic effects of aqueous extracts from reunionese medicinal plants: Insights from zebrafish models.

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie·2025
Same author

Urinary peptide signature distinguishes autosomal recessive polycystic kidney disease from other causes of chronic kidney disease.

Clinical kidney journal·2025
Same author

Development and Validation of a Capillary Electrophoresis Coupled to Mass Spectrometry Pipeline for Comparable Assessment of the Plasma Peptidome.

Proteomics·2025

Related Experiment Video

Updated: Jun 21, 2026

A Murine Model of Irreversible and Reversible Unilateral Ureteric Obstruction
14:05

A Murine Model of Irreversible and Reversible Unilateral Ureteric Obstruction

Published on: December 20, 2014

Obstructive nephropathy: insights from genetically engineered animals.

Jean-Loup Bascands1, Joost P Schanstra

  • 1Inserm U388, Institut Louis Bugnard, Touluse cedex, France.

Kidney International
|August 18, 2005
PubMed
Summary

Genetically modified animals reveal complex roles for molecules like Angiotensin II in pediatric obstructive nephropathy, a leading cause of kidney failure. Further research may uncover new antifibrotic therapies for this condition.

More Related Videos

A Mouse 5/6th Nephrectomy Model That Induces Experimental Uremic Cardiomyopathy
07:52

A Mouse 5/6th Nephrectomy Model That Induces Experimental Uremic Cardiomyopathy

Published on: November 7, 2017

5/6 Nephrectomy Using Sharp Bipolectomy Via Midline Laparotomy in Rats
05:34

5/6 Nephrectomy Using Sharp Bipolectomy Via Midline Laparotomy in Rats

Published on: April 4, 2025

Related Experiment Videos

Last Updated: Jun 21, 2026

A Murine Model of Irreversible and Reversible Unilateral Ureteric Obstruction
14:05

A Murine Model of Irreversible and Reversible Unilateral Ureteric Obstruction

Published on: December 20, 2014

A Mouse 5/6th Nephrectomy Model That Induces Experimental Uremic Cardiomyopathy
07:52

A Mouse 5/6th Nephrectomy Model That Induces Experimental Uremic Cardiomyopathy

Published on: November 7, 2017

5/6 Nephrectomy Using Sharp Bipolectomy Via Midline Laparotomy in Rats
05:34

5/6 Nephrectomy Using Sharp Bipolectomy Via Midline Laparotomy in Rats

Published on: April 4, 2025

Area of Science:

  • Nephrology
  • Pediatric Nephrology
  • Molecular Biology
  • Animal Models

Background:

  • Congenital obstructive nephropathy is a major cause of end-stage renal disease (ESRD) in children.
  • Unilateral ureteral obstruction (UUO) is an established animal model for studying obstructive nephropathy and its progression to tubulointerstitial fibrosis.
  • Genetically modified animal models have become crucial tools for dissecting the molecular mechanisms underlying obstructive nephropathy.

Purpose of the Study:

  • To investigate the role of specific gene products in the pathogenesis of obstructive nephropathy using genetically modified animal models.
  • To elucidate the complex molecular pathways involved in tubulointerstitial fibrosis during obstructive nephropathy.
  • To identify potential therapeutic targets for antifibrotic strategies.

Main Methods:

  • Utilizing genetically modified animal models, primarily knockouts, to study obstructive nephropathy.
  • Analyzing the accelerated stages of nephropathy, including cellular infiltration, apoptosis, epithelial-mesenchymal transition (EMT), and extracellular matrix (ECM) deposition.
  • Employing pharmacologic tools in conjunction with genetically modified animals to explore molecular functions.

Main Results:

  • Confirmed the significant pathological roles of angiotensin II (Ang II) and transforming growth factor-beta (TGF-beta) in obstructive nephropathy.
  • Revealed complex and sometimes contradictory roles for Ang II, matrix metalloproteinase 9 (MMP-9), tissue plasminogen activators (PAs), plasminogen activator inhibitor 1 (PAI-1), and osteopontin (OPN).
  • Highlighted the involvement of numerous functionally related molecules in the development of tubulointerstitial fibrosis.

Conclusions:

  • Genetically modified animals provide valuable insights into the pathogenesis of obstructive nephropathy, despite some limitations.
  • The study identified unexpected dual roles (pro- and antifibrotic) for key molecules in fibrotic kidney disease.
  • Further research with these models and pharmacologic agents is essential for developing effective antifibrotic therapies for obstructive nephropathy.