4.6 Review

Corin: A Key Mediator in Sodium Homeostasis, Vascular Remodeling, and Heart Failure

Journal

BIOLOGY-BASEL
Volume 11, Issue 5, Pages -

Publisher

MDPI
DOI: 10.3390/biology11050717

Keywords

apical membrane trafficking; atrial natriuretic peptide; corin; eccrine sweat glands; heart failure; protease; renal epithelial cells; sodium homeostasis; spiral artery remodeling

Categories

Funding

  1. National Natural Science Foundation of China [81873840, 32171112, 81873566]
  2. Priority Academic Program Development of Jiangsu Higher Education Institutes

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ANP is a crucial hormone that plays a key role in regulating various physiological and pathological processes. Corin, a transmembrane protease, activates ANP and is associated with cardiovascular disease. Recent studies indicate that corin-mediated ANP production and signaling are important for maintaining cardiovascular homeostasis.
Simple Summary Atrial natriuretic peptide (ANP) is an important hormone that regulates many physiological and pathological processes, including electrolyte and body fluid balance, blood volume and pressure, cardiac channel activity and function, inflammatory response, lipid metabolism, and vascular remodeling. Corin is a transmembrane serine protease that activates ANP. Variants in the CORIN gene are associated with cardiovascular disease, including hypertension, cardiac hypertrophy, atrial fibrillation, heart failure, and preeclampsia. The current data indicate a key role of corin-mediated ANP production and signaling in the maintenance of cardiovascular homeostasis. In this review, we discuss the latest findings regarding the molecular and cellular mechanisms underlying the role of corin in sodium homeostasis, uterine spiral artery remodeling, and heart failure. Atrial natriuretic peptide (ANP) is a crucial element of the cardiac endocrine function that promotes natriuresis, diuresis, and vasodilation, thereby protecting normal blood pressure and cardiac function. Corin is a type II transmembrane serine protease that is highly expressed in the heart, where it converts the ANP precursor to mature ANP. Corin deficiency prevents ANP activation and causes hypertension and heart disease. In addition to the heart, corin is expressed in other tissues, including those of the kidney, skin, and uterus, where corin-mediated ANP production and signaling act locally to promote sodium excretion and vascular remodeling. These results indicate that corin and ANP function in many tissues via endocrine and autocrine mechanisms. In heart failure patients, impaired natriuretic peptide processing is a common pathological mechanism that contributes to sodium and body fluid retention. In this review, we discuss most recent findings regarding the role of corin in non-cardiac tissues, including the kidney and skin, in regulating sodium homeostasis and body fluid excretion. Moreover, we describe the molecular mechanisms underlying corin and ANP function in supporting orderly cellular events in uterine spiral artery remodeling. Finally, we assess the potential of corin-based approaches to enhance natriuretic peptide production and activity as a treatment of heart failure.

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