Complete loss of the atrial natriuretic peptide‐converting enzyme Corin and CHAF‐LA syndrome: Implications to natriuretic peptide physiology and left atrium health

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The natriuretic peptide (NP) hormone system has been extensively studied in the context of blood pressure homeostasis and cardiovascular disease. 1 Two main NPs -atrial natriuretic peptide (ANP) and B-type/ brain NP (BNP)are secreted from the left atrial and ventricular cardiomyocytes, respectively, following stimuli, such as fluid overload, sympathetic stimulation, and hypernatremia. 1 ANP and BNP are synthesized in cardiomyocytes as preprohormones, where they are cleaved to produce prohormones.These prohormones -proANP and proBNPundergo additional proteolytic cleavage by the transmembrane enzymes Corin and Furin to remove the N-terminal region and form the mature and active hormones, which are released to the bloodstream (Figure 1). 1 Interestingly, while proBNP can be cleaved by both Furin and Corin, proANP is cleaved exclusively by Corin. 1 ANP and BNP exert their physiological responses through binding NPR-A (also known as GC-A) receptors and activating cGMP signaling in target organs (Figure 1), where they promote vasodilation (in blood vessels), natriuresis and diuresis (in the kidney), inhibit the renin-angiotensin-aldosterone pathway, and protect against hypertrophy, fibrosis and apoptosis (in the heart).1,2 Due to their similar struc-

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