cathepsin-g and Cardiac-Output--Low

cathepsin-g has been researched along with Cardiac-Output--Low* in 1 studies

Other Studies

1 other study(ies) available for cathepsin-g and Cardiac-Output--Low

ArticleYear
Mast cell-derived cathepsin g: a possible role in the adverse remodeling of the failing human heart.
    The Journal of surgical research, 2007, Jun-15, Volume: 140, Issue:2

    The role of cardiac mast cells (MCs) in the progression to heart failure has recently become increasingly evident. Cathepsin g is a neutrophil- and mast cell-derived protease, which can convert angiotensin I to angiotensin II and thereby activate the TGF-beta pathway, resulting in myocyte necrosis, hypertrophy, and increased fibrosis. This study focuses on mast cell-derived cathepsin g in the human heart during heart failure and following mechanical unloading by means of heart-assist devices (LVADs).. Myocardial tissue was obtained from 10 patients with end-stage cardiomyopathy at the time of LVAD implantation (pre-LVAD) and following orthotopic heart transplantation (post-LAVD). In addition, biopsies of four normal hearts served as a control group. Paraffin-embedded sections were dual stained for cathepsin g and tryptase, a known marker for mast cells, using standard immunohistochemistry protocols. Total cathepsin g positive mast cells were counted.. No cathepsin g positive MCs were found in normal hearts. However, we found evidence for cathepsin g in cardiac MCs in heart failure tissues (pre-LVAD). During heart failure, 46% of total MCs were cathepsin g positive as compared to after mechanical unloading, where only 11% of total MCs were cathepsin g positive (P<0.001).. Heart failure causes an increase of myocardial MCs. We have provided evidence that cathepsin g positive MCs accumulate during heart failure and their total percentage decreases after ventricular unloading. This coincides with the decrease in myocyte necrosis, hypertrophy, and fibrosis. Thus, cathepsin g may play a role in the progression to heart failure by activating angiotensin II, leading to detrimental effects on the heart.

    Topics: Adult; Aged; Angiotensin II; Cardiac Output, Low; Case-Control Studies; Cathepsin G; Cathepsins; Chymases; Disease Progression; Female; Heart-Assist Devices; Humans; Male; Mast Cells; Middle Aged; Myocardium; Necrosis; Serine Endopeptidases; Tryptases; Ventricular Remodeling

2007