Cardiac fibroblasts: friend or foe?
- 1 September 2006
- journal article
- review article
- Published by American Physiological Society in American Journal of Physiology-Heart and Circulatory Physiology
- Vol. 291 (3) , H1015-H1026
- https://doi.org/10.1152/ajpheart.00023.2006
Abstract
Cardiac function is determined by the dynamic interaction of various cell types and the extracellular matrix that composes the heart. This interaction varies with the stage of development and the degree and duration of mechanical, chemical, and electrical signals between the various cell types and the ECM. Understanding how these complex signals interact at the molecular, cellular, and organ levels is critical to understanding the function of the heart under a variety of physiological and pathophysiological conditions. Quantitative approaches, both in vivo and in vitro, are essential to understand the dynamic interaction of mechanical, chemical, and electrical stimuli that govern cardiac function. The fibroblast can thus be a friend in normal function or a foe in pathophysiological conditions.Keywords
This publication has 158 references indexed in Scilit:
- Matrikines in the regulation of extracellular matrix degradationBiochimie, 2005
- Angiotensin II induces focal adhesion kinase/paxillin phosphorylation and cell migration in human umbilical vein endothelial cellsBiochemical and Biophysical Research Communications, 2005
- Effects of collagen density on cardiac fibroblast behavior and gene expressionJournal of Cellular Physiology, 2003
- Stretch-activated pathways and left ventricular remodelingJournal of Cardiac Failure, 2002
- Myofibroblasts and mechano-regulation of connective tissue remodellingNature Reviews Molecular Cell Biology, 2002
- Is angiotensin II a proliferative factor of cardiac fibroblasts?Cardiovascular Research, 2002
- Uniaxial Cyclic Stretch Induces Focal Adhesion Kinase (FAK) Tyrosine Phosphorylation Followed by Mitogen-Activated Protein Kinase (MAPK) ActivationBiochemical and Biophysical Research Communications, 2001
- AP-1 in cell proliferation and survivalOncogene, 2001
- Ras/MEK/ERK Up-regulation of the Fibroblast KCaChannel FIK Is a Common Mechanism for Basic Fibroblast Growth Factor and Transforming Growth Factor-β Suppression of MyogenesisJournal of Biological Chemistry, 2000
- Time‐dependent increases in type‐III collagen gene expression in medial collateral ligament fibroblasts under cyclic strainsJournal of Orthopaedic Research, 2000