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Updated: May 8, 2026

Processing of Human Cardiac Tissue Toward Extracellular Matrix Self-assembling Hydrogel for In Vitro and In Vivo Applications
Published on: December 4, 2017
BNP molecular forms and processing by the cardiac serine protease corin
Tomoko Ichiki1, Brenda K Huntley, John C Burnett
1Cardiorenal Research Laboratory, Division of Cardiovascular Diseases, Mayo Clinic, Rochester, Minnesota, USA. ichiki.tomoko@mayo.edu
B-type natriuretic peptide (BNP) is a cardiac hormone used for heart failure (HF). Paradoxical elevations in inactive BNP forms in HF suggest impaired processing, potentially involving the corin convertase.
Area of Science:
- Biochemistry
- Cardiology
- Molecular Biology
Background:
- B-type natriuretic peptide (BNP) is a cardiac hormone with cardiorenal protective functions, crucial as a biomarker and therapeutic agent for heart failure (HF).
- Prohormone proBNP1_108 is processed into inactive NT-proBNP1_76 and active BNP1-32 by corin or furin convertases.
- Elevated circulating NT-proBNP and BNP in HF present a paradox, possibly due to non-specific assays or a deficiency in active BNP relative to inactive forms.
Purpose of the Study:
- To investigate the regulation of proBNP1_108 processing and the role of the corin convertase in the physiology of heart failure.
- To explore the potential link between impaired proBNP1_108 processing in HF and dysregulation of the corin convertase.
Main Methods:
- Analysis of proBNP1_108 processing by corin and furin convertases.
- Investigation of corin expression in cardiac and renal tissues.
- Exploration of O-linked glycosylation's role in controlling proBNP1_108 processing by corin.
Main Results:
- Corin, expressed in the heart and kidney, plays a role in regulating blood pressure and cardiac remodeling.
- O-linked glycosylation may control proBNP1_108 processing by corin.
- Impaired proBNP1_108 processing in HF might be associated with corin dysregulation.
Conclusions:
- Understanding proBNP1_108 processing and corin's function is vital for comprehending HF pathophysiology.
- Corin dysregulation in HF may present therapeutic targets for controlling proBNP processing and activation.
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