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Chymase Inhibition Prevents Fibronectin and Myofibrillar Loss and Improves Cardiomyocyte Function and LV Torsion Angle in Dogs With Isolated Mitral Regurgitation
Author(s) -
Betty Pat,
Yuanwen Chen,
Cheryl R. Killingsworth,
James D. Gladden,
Ke Shi,
Junying Zheng,
Pamela C. Powell,
Greg Walcott,
Mustafa I. Ahmed,
Himanshu Gupta,
Ravi Desai,
ChihChang Wei,
Naoki Hase,
Tsunefumi Kobayashi,
Abdelkarim Sabri,
Henk Granzier,
Thomas S. Denney,
Michael Tillson,
A. Ray Dillon,
Ahsan Husain,
Louis J. Dell’Italia
Publication year - 2010
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/circulationaha.109.921619
Subject(s) - fibronectin , myofibril , medicine , extracellular matrix , chymase , phosphorylation , endocrinology , cardiology , biology , microbiology and biotechnology , immunology , mast cell
The left ventricular (LV) dilatation of isolated mitral regurgitation (MR) is associated with an increase in chymase and a decrease in interstitial collagen and extracellular matrix. In addition to profibrotic effects, chymase has significant antifibrotic actions because it activates matrix metalloproteinases and kallikrein and degrades fibronectin. Thus, we hypothesize that chymase inhibitor (CI) will attenuate extracellular matrix loss and LV remodeling in MR.

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