Multifunctional Role of Chymase in Acute and Chronic Tissue Injury and Remodeling

Chymase is the most efficient Ang II (angiotensin II)–forming enzyme in the human body and has been implicated in a wide variety of human diseases that also implicate its many other protease actions. Largely thought to be the product of mast cells, the identification of other cellular sources includ...

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Bibliographic Details
Published in:Circulation research 2018-01, Vol.122 (2), p.319-336
Main Authors: Dell’Italia, Louis J, Collawn, James F, Ferrario, Carlos M
Format: Article
Language:English
Subjects:
Acute Disease
Angiotensin
Angiotensin II
Angiotensin II - metabolism
Angiotensin Receptor Antagonists - pharmacology
Angiotensin Receptor Antagonists - therapeutic use
Animals
Cardiomyocytes
Cardiovascular Diseases - drug therapy
Cardiovascular Diseases - enzymology
Cardiovascular Diseases - pathology
Chronic Disease
Chymase
Chymases - antagonists & inhibitors
Chymases - physiology
Clinical trials
Endothelial cells
Enzyme Inhibitors - pharmacology
Enzyme Inhibitors - therapeutic use
Fibroblasts
Heart diseases
Humans
Mast cells
Mast Cells - metabolism
Renin
Renin-Angiotensin System - drug effects
Renin-Angiotensin System - physiology
Smooth muscle
Vascular Remodeling - drug effects
Vascular Remodeling - physiology
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Summary:Chymase is the most efficient Ang II (angiotensin II)–forming enzyme in the human body and has been implicated in a wide variety of human diseases that also implicate its many other protease actions. Largely thought to be the product of mast cells, the identification of other cellular sources including cardiac fibroblasts and vascular endothelial cells demonstrates a more widely dispersed production and distribution system in various tissues. Furthermore, newly emerging evidence for its intracellular presence in cardiomyocytes and smooth muscle cells opens an entirely new compartment of chymase-mediated actions that were previously thought to be limited to the extracellular space. This review illustrates how these multiple chymase-mediated mechanisms of action can explain the residual risk in clinical trials of cardiovascular disease using conventional renin–angiotensin system blockade.
ISSN:0009-7330
1524-4571
DOI:10.1161/CIRCRESAHA.117.310978