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Corin is a type II transmembrane serine protease primarily expressed in cardiac myocytes, where it is essential for the conversion of the precursor pro-atrial natriuretic peptide (pro-ANP) into active atrial natriuretic peptide (ANP)[1][2][3][4][5]. ANP is a key hormone that promotes sodium excretion, vasodilation, and regulation of blood pressure and volume. Dysfunctional corin activity—due to genetic variants, mutations, or altered expression—is implicated in hypertensive disorders, heart failure, preeclampsia, and other cardiovascular and pregnancy-related diseases[2][3][5]. Soluble forms of corin, released into circulation, are being investigated as biomarkers for cardiovascular diseases and preeclampsia[3]. While corin is not currently the direct target of approved pharmacological interventions, its central role in cardiac and vascular homeostasis makes it a focus of basic and translational research, especially regarding the natriuretic peptide axis and cardiovascular risk stratification[3][5].
Augmentation of natriuretic peptide signaling (by increasing bioavailable ANP/BNP, not by directly acting on corin). - Inhibition of neprilysin to prevent natriuretic peptide degradation (indirectly increases the clinical effect of corin activity).
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