Role of corin in the regulation of blood pressure

Abstract

Purpose of review Corin is a transmembrane protease that activates atrial natriuretic peptide (ANP), an important hormone in regulating salt-water balance and blood pressure. This review focuses on the regulation of corin function and potential roles of corin defects in hypertensive, heart, and renal diseases. Recent findings Proprotein convertase subtilisin/kexin-6 has been identified as a primary enzyme that converts zymogen corin to an active protease. Genetic variants that impair corin intracellular trafficking, cell surface expression, and zymogen activation have been found in patients with hypertension, cardiac hypertrophy, and pre-eclampsia. Reduced corin expression has been detected in animal models of cardiomyopathies and in human failing hearts. Low levels of circulating soluble corin have been reported in patients with heart disease and stroke. Corin, ANP and natriuretic peptide receptor-A mRNAs, and proteins have been colocalized in human renal segments, suggesting a corin-ANP autocrine function in the kidney. Summary Corin is a key enzyme in the natriuretic peptide system. The latest findings indicate that corin-mediated ANP production may act in a tissue-specific manner to regulate cardiovascular and renal function. Corin defects may contribute to major diseases such as hypertension, heart failure, pre-eclampsia, and kidney disease

Single Cell Profiling Reveals Sex, Lineage and Regional Diversity in the Mouse Kidney

“…Examining disease linkage, Corin expression, which is quite specific to the cortical nephron-specific cell population, encodes a serine peptidase critical to the regulation of blood volume and blood pressure. Human variants in Corin are linked to hypertension, cardiac hypertrophy and pre-eclampsia (Li et al, 2017).…”

N-glycosylation in the protease domain of trypsin-like serine proteases mediates calnexin-assisted protein folding

“…Corin is a trypsin-like serine protease that activates natriuretic peptides ( Cui et al, 2012 ; Li et al, 2017 ; Yan et al, 2000 ). It consists of a cytoplasmic tail, a transmembrane domain and an extracellular region with multiple protein modules and a C-terminal protease domain ( Hooper et al, 2000 ; Yan et al, 1999 ).…”

Effect of Improving Volume Overload on Home Blood Pressure Variability in Hemodialysis Patients

“…Although it was not detected in the present study, several researches in vivo and in vitro have demonstrated that excessive fluid volume would cause cardiomyocyte injury and apoptosis, which could induce a series of cardiovascular dysfunctions by impairing biochemical signal transduction, vascular tone adaptation, and baroreflex control of circulation . When HD patients are fluid overloaded, the sustained preload‐induced cardiomyocyte injury might lead to abnormal expression and production of bioactive substances that could disrupt BP regulation . However, the exact mechanism involved was not yet adequately established.…”