Matrix metalloproteinases and their tissue inhibitors in pressure-overloaded human myocardium during heart failure progression

• Published in: Journal of the American College of Cardiology 2004-10, Vol.44 (8), p.1609-1618
• Main Authors: Polyakova, Victoria, Hein, Stefan, Kostin, Sawa, Ziegelhoeffer, Tibor, Schaper, Jutta
• Format: Article
• Language: English
• Subjects: Aged; Aortic Valve Stenosis - pathology; Aortic Valve Stenosis - surgery; Binding sites; Biological and medical sciences; Biopsy; Cardiology; Cardiology. Vascular system; Cell Division - physiology; Collagen; Disease Progression; Endocardium - pathology; Endomyocardial Fibrosis - pathology; Enzymes; Extracellular Matrix - pathology; Female; Fibroblasts - pathology; Heart; Heart failure; Heart Failure - pathology; Heart failure, cardiogenic pulmonary edema, cardiac enlargement; Heart Valve Prosthesis Implantation; Humans; Hypertrophy, Left Ventricular - pathology; Male; Matrix Metalloproteinases - metabolism; Medical sciences; Microscopy; Microscopy, Fluorescence; Middle Aged; Myocardium - pathology; Protein Isoforms - metabolism; Reference Values; Rodents; Smooth muscle; Software; Tissue Inhibitor of Metalloproteinases - metabolism; Ventricular Remodeling - physiology
• ISSN: 0735-1097; 1558-3597
• DOI: 10.1016/j.jacc.2004.07.023

We studied the role of matrix metalloproteinases (MMPs) and their tissue inhibitors (TIMPs) in fibrosis formation in the transition from hypertrophy to heart failure (HF) as well as the cellular source of MMPs and TIMPs. Human pressure-overloaded hearts are characterized by a significant increase in cardiac fibrosis. However, the contribution of the proteolytic/antiproteolytic system in aortic stenosis (AS) during hypertrophy progression has not yet been elucidated. Three groups of AS patients (I: EF >50%, n = 12; II: EF 50% to 30%, n = 10; III: EF