Corin is a type II transmembrane serine protease. Its essential function is to convert the atrial natriuretic peptide (ANP) precursor to mature ANP. This process is crucial for maintaining electrolyte balance, normal blood pressure, and cardiac function, as ANP promotes natriuresis, diuresis, and vasodilation. The PI3K/AKT and NF-κB signaling pathways are associated with Corin's function in protecting cardiomyocytes [1]. Genetic models, such as knockout mice, have been valuable in studying Corin.

In Corin knockout (KO) mice, fecal Na+ and Cl- excretion decreased compared with wild-type mice, suggesting that intestinal corin may promote fecal sodium excretion in a paracrine mechanism independent of cardiac corin function [4]. In mice lacking corin, the conversion of pro-ANP to ANP is prevented, leading to salt-sensitive hypertension, which is exacerbated during pregnancy [2]. Also, in two siblings with a homozygous null variant in CORIN, they presented with cardiomyopathy, hypertension, arrhythmia, and fibrosis of the left atrium, supporting the importance of corin to normal ANP activity, left atrial function, and cardiovascular homeostasis [3].

In conclusion, Corin is a key mediator in sodium homeostasis, vascular remodeling, and heart function. Studies using KO mouse models have revealed its role in various biological processes and disease conditions, such as hypertension, heart failure, and left atrial cardiomyopathy. Understanding Corin's function contributes to a better understanding of the mechanisms underlying these diseases and may offer potential therapeutic targets.