Copyright © 2005, European Society of Cardiology
Pathways of matrix metalloproteinase induction in heart failure: Bioactive molecules and transcriptional regulation
Division of Cardiothoracic Surgery, Medical University of South Carolina, 114 Doughty Street, Room 625, Strom Thurmond Research Building, Charleston, SC 29403, United States
The Ralph H. Johnson Veteran's Association Medical Center, United States
* Corresponding author. Division of Cardiothoracic Surgery, Medical University of South Carolina, 114 Doughty Street, Room 625, Strom Thurmond Research Building, Charleston, SC 29403, United States. Tel.: +1 843 876 5186; fax: +1 843 876 5187. Email address: wilburnm{at}musc.edu
The structural basis for the development of congestive heart failure (CHF) is a maladaptive myocardial remodeling process which occurs secondarily to post-myocardial infarction (MI), hypertensive hypertrophy, or cardiomyopathy. Both cellular and extracellular factors are involved in the remodeling process and it is the combined action of these factors giving rise to changes in myocardial structure which eventually affects function. One component in this remodeling process is a family of extracellular matrix degrading enzymes, the matrix metalloproteinases or MMPs. Many bioactive molecules such as cytokines/chemokines, bioactive peptides, and neurohormones which are operative in CHF likely contribute to the induction of MMPs. For example, a specific cassette of transcription factors is likely induced with extracellular stimuli in the context of CHF which in turn induces MMPs and contributes to the maladaptive remodeling process. This review will briefly discuss the biology of the MMP family, but will more importantly identify how biological factors active in CHF result in the modulation of the MMP family. Understanding how upstream molecules are involved in MMP regulation/dysregulation may provide an avenue to develop important therapeutic interventions.
KEYWORDS Transcriptional regulation; Matrix metalloproteinases; Promoter
Abbreviations: CHF, congestive heart failure • LV, left ventricle (ventricular) • MMP, matrix metalloproteinase • MT-MMP, membrane-type MMP • TIMP, tissue inhibitor of metalloproteinases • mRNA, messenger ribonucleic acid • TNF, tumor necrosis factor-alpha • TGF-β, transforming growth factor-beta • Ang II, angiotensin II • ET, endothelin-1 • IL-1β, interleukin-1beta • OPN, osteopontin • TSP, thrombospondin • NF-
B, nuclear factor kappa B • AP-1, activator protein-1 • PEA-3, polyoma enhancer A binding protein-3 • TIE, TGF-β inhibitory elements • STAT, signal transducers and activators of transcription • JAK, Janus kinase • PKC, protein kinase c • TRADD, TNFR1-associated death domain protein • RIP1, receptor interacting protein a • FADD, fas-associated death domain protein • TRAF2, TNF receptor-associated factor 2 • EGF, epidermal growth factor • ROS, reactive oxygen species
Time for primary review 25 days
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