title: Disruptions and detours in the myocardial matrix highway and heart failure.
abstract: Myocardial remodeling invariably occurs in congestive heart failure (CHF) and is a response to a prolonged cardiovascular stress, which is characterized by a cascade of compensatory structural events. Remodeling of the myocardial interstitium occurs in CHF and likely contributes to the progression of the remodeling process. The myocardial matrix can be considered a biological highway in which a large amount of signaling proteins and structural proteins are being moved within the interstitium, entering and exiting the interstitial space, and docking to cellular components. The rates at which these events occur can accelerate and decelerate depending on the particular cardiac disease state and thereby can alter the course of myocardial remodeling. Once considered merely a scaffolding to align cells, the matrix plays a complex and divergent role in influencing cell behavior. For example, the matrix has a functional role in cell migration, proliferation, adhesion, and cell-to-cell signaling. In light of this, the myocardial matrix should not be regarded as merely a static structure, but rather, as a complex system of dynamic interactions between matrix molecules, signaling proteins, and transmembrane proteins. Specific strategies that are targeted at modifying activity along this matrix highway will likely alter the course of myocardial remodeling and heart failure.
authors.affiliation: Cardiothoracic Surgery, Medical University of South Carolina, 114 Doughty Street, Room 625, Strom Thurmond Research Building, Charleston, SC 29403, USA.
authors.forename: Anne M
authors.initials: AM
authors.lastname: Deschamps
authors.forename: Francis G
authors.initials: FG
authors.lastname: Spinale
mesh_terms: D000804:Angiotensin II / Q000502:physiology; D018450:Disease Progression; D019332:Endothelin-1 / Q000502:physiology; D005109:Extracellular Matrix / Q000378:metabolism / Q000502:physiology*; D006333:Heart Failure / Q000378:metabolism / Q000503:physiopathology*; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000503:physiopathology; D016023:Integrins / Q000502:physiology; D020782:Matrix Metalloproteinases / Q000378:metabolism*; D009203:Myocardial Infarction / Q000378:metabolism; D009206:Myocardium / Q000737:chemistry / Q000378:metabolism*; D016212:Transforming Growth Factor beta / Q000502:physiology; D020257:Ventricular Remodeling / Q000502:physiology
chemical_list: D019332:Endothelin-1; D016023:Integrins; D016212:Transforming Growth Factor beta; D000804:Angiotensin II; D020782:Matrix Metalloproteinases