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Updated: Jul 2, 2026
08:34
Isolation of Atrial Myocytes from Adult Mice
Published on: July 25, 2019
Corin: new insights into the natriuretic peptide system
Qingyu Wu1, Ye Olivia Xu-Cai, Shenghan Chen
1Department of Molecular Cardiology, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio 44195, USA. wuq@ccf.org
Kidney International
|August 22, 2008
Summary
Corin protease is crucial for converting precursor natriuretic peptides to active forms, regulating blood pressure. Corin deficiency in mice causes salt-sensitive hypertension, suggesting its role in human heart disease.
Area of Science:
- Cardiovascular physiology
- Enzymology
- Genetics
Background:
- Natriuretic peptides regulate salt and body-fluid homeostasis.
- Proteolytic processing converts precursor peptides to active forms.
- Corin is a heart-identified transmembrane serine protease.
Purpose of the Study:
- To investigate the role of corin in pro-atrial natriuretic peptide (pro-ANP) processing.
- To determine the in vivo function of corin in blood pressure regulation.
- To explore the link between corin deficiency and hypertension.
Main Methods:
- Studied corin's enzymatic activity on pro-ANP.
- Utilized a mouse model lacking functional corin.
- Observed hypertensive phenotypes in corin-deficient mice, particularly during pregnancy.
- Analyzed human genetic data for corin gene polymorphisms in hypertensive individuals.
Main Results:
- Corin specifically converts pro-ANP to active ANP.
- Corin deficiency in mice leads to salt-sensitive hypertension.
- Hypertension is worsened by pregnancy in corin-deficient mice.
- Corin gene variations are associated with hypertension and cardiac hypertrophy in humans.
Conclusions:
- Corin is essential for maintaining normal blood pressure in vivo.
- Corin deficiency is a potential contributing factor to human hypertension and heart disease.
- Targeting corin may offer therapeutic strategies for cardiovascular conditions.
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