NAME: Mary Bunten
Patients with chronic renal failure are at a higher risk for cardiovascular diseases due to the stress the heart undergoes as the kidneys lose function1. This stress on the heart results in oxidative stress with an imbalance in reactive oxygen species (ROS)12. A major result of oxidative stress is uremic cardiomyopathy which can cause several cardiovascular abnormalities specific to chronic kidney disease such as: Left Ventricle Hypertrophy (LVH), Left Ventricle (LV) dilatation, LV systolic, and diastolic dysfunction3. The cardiovascular issues which arise from uremic cardiomyopathy increase the mortality rate of patients experiencing chronic kidney failure. This research project is broken down into two studies, with the first study of the research focusing on the following two specific aims:
1) to test the effects of the drugs pNaKtide (Na+/K+ -ATPase signaling inhibitor) and Cobalt protoporphyrin (CoPP, Heme Oxygenase -1 inducer) on uremic cardiomyopathy using the mouse partial nephrectomy model ( ) to stimulate chronic kidney disease, and
2) to observe the physical condition of the heart after a four-week administration of the aforementioned drugs in mice.
In the second study of the proposed research project, we plan to observe if the cardiac fibrosis symptom of uremic cardiomyopathy can be reversed at the end-stage of renal failure using pNaKtide. pNaKtide plays an important role in preventing fibrosis which is why it was the drug chosen for the reversal study13. No emphasis will be placed on the administration of CoPP, at this point, because CoPP is known to aid blood pressure related cardiovascular issues more so than fibrosis2. At the end of this study, we hope to demonstrate if pNaKtide and CoPP can positively impact the treatment of uremic cardiomyopathy, as measured by the mortality rate due to chronic kidney failure in heart myopathies.
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