Nppa, which encodes atrial natriuretic peptide (ANP), is a crucial gene in the cardiovascular system. ANP regulates salt-water balance and blood pressure by promoting renal sodium and water excretion and stimulating vasodilation. It also has anti-hypertrophic functions in the heart independent of blood-pressure-lowering effects. The gene is involved in pathways related to cardiovascular biology, and its expression is associated with various physiological and pathological processes [3].

In mouse models, Nppa knockout mice undergoing ischemia-reperfusion (I/R) show increased infarct size and reduced autophagy, indicating that Nppa plays a role in protecting the heart during I/R injury through its regulation of autophagy [2]. In neonatal mice, deletion of the lncRNA NPPA-AS1 (associated with Nppa) prolongs the postnatal window of heart regeneration after apical resection, while in adult mice, it improves cardiac function and reduces infarct size after myocardial infarction, associated with enhanced cardiomyocyte proliferation [1].

In conclusion, Nppa is essential for maintaining cardiovascular homeostasis, especially in regulating blood pressure, heart function, and autophagy. Mouse models, including Nppa knockout and those targeting related lncRNAs like NPPA-AS1, have revealed its significance in heart-related diseases such as myocardial infarction and cardiac regeneration, providing insights into potential therapeutic targets for cardiovascular disorders.