## Abstract Cardiac fibroblasts (CF) play a key role in orchestrating the structural remodeling of the myocardium in response to injury or stress, in part through direct regulation of extracellular matrix (ECM) turnover. The matrix metalloproteinases (MMPs) are a family of over 25 zincβdependent pr
Regulation of myocardial matrix metalloproteinase expression and activity by cardiac fibroblasts
β Scribed by Neil A. Turner; Karen E. Porter
- Publisher
- John Wiley and Sons
- Year
- 2012
- Tongue
- English
- Weight
- 124 KB
- Volume
- 64
- Category
- Article
- ISSN
- 1521-6543
- DOI
- 10.1002/iub.1004
No coin nor oath required. For personal study only.
β¦ Synopsis
Abstract
Cardiac fibroblasts (CF) play a key role in orchestrating the structural remodeling of the myocardium in response to injury or stress, in part through direct regulation of extracellular matrix (ECM) turnover. The matrix metalloproteinases (MMPs) are a family of over 25 zincβdependent proteases that together have the capacity to degrade all the protein components of the ECM. Fibroblasts are a major source of several MMPs in the heart, thereby representing a viable therapeutic target for regulating ECM turnover in cardiac pathologies characterized by adverse remodeling, such as myocardial infarction, cardiomyopathy, hypertension and heart failure. This review summarizes current knowledge on the identity and regulation of MMPs expressed by CF and discusses future directions for reducing adverse myocardial remodeling by modulating the expression and/or activity of CFβderived MMPs. Β© 2012 IUBMB IUBMB Life, 2012.
π SIMILAR VOLUMES
## Abstract The metalloproteinases degrade extracellular matrix (ECM) components and activate growth factors, thereby contributing to physiological events (tissue remodeling in pregnancy, wound healing, angiogenesis) and pathological conditions (cancer, arthritis, periodontitis). The intent of this
In the normal heart, cardiomyocytes are surrounded by extracellular matrix (ECM) and latent matrix metalloproteinases (MMPs), which are produced primarily by cardiac fibroblasts. An activator of latent MMPs might be induced by ischemic conditions or pressure-induced stretching. To test the hypothesi
## Abstract Fibroblasts, a major constituent of gingival connective tissue, can produce immunoregulatory cytokines and proteolytic enzymes that may contribute to tissue destruction. In this study, we evaluated the production of matrix metalloproteinases (MMPs), tissue inhibitors of MMPs (TIMPs), an
## Abstract ## Objective To evaluate the effects of LG100268 (LG268), a synthetic ligand for the nuclear hormone receptor retinoid X receptor, on the expression of matrix metalloproteinase 1 (MMPβ1) and MMPβ13 induced by proinflammatory cytokines in a chondrocyte model. ## Methods SWβ1353 human
## Abstract Matrix metalloproteinases (MMPs) degrade the extracellular matrix and are implicated in the pathogenesis of several neurological diseases. Secreted in proforms, the MMPs require activation. Tissue inhibitors of matrix metalloproteinases (TIMPs) regulate the activity of MMPs. We investig