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Updated: Mar 5, 2026

A Mouse 5/6th Nephrectomy Model That Induces Experimental Uremic Cardiomyopathy
Published on: November 7, 2017
Sodium potassium adenosine triphosphatase (Na/K-ATPase) as a therapeutic target for uremic cardiomyopathy
Xiaoliang Wang1,2, Jiang Liu1, Christopher A Drummond2
1a Joan C Edwards School of Medicine at Marshall University , Huntington , WV , United States.
Insights
Uremic cardiomyopathy, common in chronic kidney disease, involves heart dysfunction. Targeting the Na/K-ATPase/Src/ROS amplification loop offers a promising new therapeutic strategy for this condition.
Area of Science:
- Cardiovascular Medicine
- Nephrology
- Molecular Biology
Background:
- Uremic cardiomyopathy is a common cardiovascular complication in patients with chronic kidney disease (CKD).
- It is characterized by progressive cardiac changes, including diastolic dysfunction, hypertrophy, and potentially systolic dysfunction.
- This condition is nearly universal in end-stage renal disease (ESRD).
Purpose of the Study:
- To review the epidemiology and pathophysiology of uremic cardiomyopathy.
- To explore the role of the Na/K-ATPase/Src/ROS amplification loop in its development.
- To discuss potential therapeutic strategies targeting this loop.
Main Methods:
- Review of recent epidemiological data.
- Analysis of the pathophysiology of uremic cardiomyopathy.
- Detailed examination of the Na/K-ATPase/Src/ROS amplification loop mechanism.
- Presentation of clinical and preclinical evidence.
- Discussion of a novel therapeutic peptide.
Main Results:
- The Na/K-ATPase/Src/ROS amplification loop is implicated in the pathogenesis of uremic cardiomyopathy.
- Clinical and preclinical studies support the role of this loop.
- A therapeutic peptide targeting this loop shows potential.
Conclusions:
- Current treatments for uremic cardiomyopathy are inadequate.
- Targeting the Na/K-ATPase/Src/ROS amplification loop presents a novel therapeutic avenue.
- Further research into Na/K-ATPase regulation is crucial for developing new treatments.
Introduction:
Clinically, patients with significant reductions in renal function present with cardiovascular dysfunction typically termed, uremic cardiomyopathy. It is a progressive series of cardiac pathophysiological changes, including left ventricular diastolic dysfunction and hypertrophy (LVH) which sometimes progress to left ventricular dilation (LVD) and systolic dysfunction in the setting of chronic kidney disease (CKD). Uremic cardiomyopathy is almost ubiquitous in patients afflicted with end stage renal disease (ESRD). Areas covered: This article reviews recent epidemiology, pathophysiology of uremic cardiomyopathy and provide a board overview of Na/K-ATPase research with detailed discussion on the mechanisms of Na/K-ATPase/Src/ROS amplification loop. We also present clinical and preclinical evidences as well as molecular mechanism of this amplification loop in the development of uremic cardiomyopathy. A potential therapeutic peptide that targets on this loop is discussed. Expert opinion: Current clinical treatment for uremic cardiomyopathy remains disappointing. Targeting the ROS amplification loop mediated by the Na/K-ATPase signaling function may provide a novel therapeutic target for uremic cardiomyopathy and related diseases. Additional studies of Na/K-ATPase and other strategies that regulate this loop will lead to new therapeutics.
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