Related Experiment Video
Updated: Oct 26, 2025
07:52
A Mouse 5/6th Nephrectomy Model That Induces Experimental Uremic Cardiomyopathy
Published on: November 7, 2017
21.2K
Uraemic Cardiomyopathy in Different Mouse Models.
Cheng Chen1,2, Caidie Xie1, Hanzhang Wu1
1Department of Nephrology, Jiangsu Province Hospital, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Frontiers in Medicine
|August 2, 2021
Summary
This study compared four mouse models for uraemic cardiomyopathy (UCM), a complication of chronic kidney disease (CKD). Results show distinct features, mortality rates, and cardiac changes across models, with GDF-15 levels decreasing in UCM mice.
Area of Science:
- Nephrology
- Cardiology
- Translational Medicine
Background:
- Uraemic cardiomyopathy (UCM) is a frequent complication in chronic kidney disease (CKD).
- Understanding UCM pathogenesis requires robust animal models.
- This study evaluates four distinct mouse models for UCM.
Purpose of the Study:
- To compare the phenotypical characteristics, mortality, and cardiac alterations of four established UCM mouse models.
- To assess the expression of Fibroblast Growth Factor 23 (FGF-23) and Growth Differentiation Factor 15 (GDF-15) in these models.
Main Methods:
- Four CKD models were established: 5/6 nephrectomy (5/6Nx), ischemia-reperfusion (IR), adenine diet, and surgical pole ligation.
- Mice were analyzed at various time points (4, 8, 16 weeks) for cardiac structure, function, and FGF-23/GDF-15 expression.
- Mortality rates were compared across the different modeling groups.
Main Results:
- The 5/6Nx model exhibited significantly higher mortality.
- Cardiac hypertrophy was observed in adenine, 5/6Nx, ligation, and IR groups.
- Cardiac fibrosis was present in all CKD models, being more severe in the IR and adenine groups.
- GDF-15 levels were downregulated in all UCM models compared to sham controls, while FGF-23 levels showed no significant difference.
Conclusions:
- The four UCM mouse models display diverse phenotypical features, development timelines, and mortality profiles.
- Cardiac fibrosis and hypertrophy are common hallmarks across these models.
- Downregulation of GDF-15 is a consistent finding in UCM mouse hearts, suggesting its potential role in UCM pathophysiology.
