Key result
Animal models demonstrate that genetic perturbation of the natriuretic peptide system causes cardiovascular disease, and exogenous administration has therapeutic potential for heart failure.
Animal models highlight the critical role of the natriuretic peptide system in cardiovascular homeostasis and its therapeutic potential in heart failure and acute coronary syndromes.
Supports exploration of natriuretic peptide modulation for heart failure; leaves open clinical translation from animal models.
Natriuretic peptides play a major role in cardiovascular homeostasis, and much of our knowledge on this stems from animal studies looking into the genetic knockout or overexpression of natriuretic peptides or their biological target, the natriuretic peptide receptor. Genetic perturbation of the natriuretic peptide system in rodents causes systemic hypertension, cardiac fibrosis, left ventricular hypertrophy, and heart failure. Moreover, animal models of acute myocardial infarction and heart failure have demonstrated the therapeutic potential of exogenously administered natriuretic peptides in treating human acute coronary syndromes and heart failure. In this review, we hope to highlight the importance of animal models in helping us understand the biological function and consequence of the natriuretic peptide system in cardiovascular disease.
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Burley et al. (2014) conducted a review in Cardiovascular disease. Natriuretic peptides was evaluated. Animal models demonstrate that genetic perturbation of the natriuretic peptide system causes cardiovascular disease, and exogenous administration has therapeutic potential for heart failure.
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