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Pathways of matrix metalloproteinase induction in heart failure: bioactive molecules and transcriptional regulation
Anne M Deschamps1, Francis G Spinale
1Division of Cardiothoracic Surgery, Medical University of South Carolina, 114 Doughty Street, Room 625, Strom Thurmond Research Building, Charleston, SC 29403, USA.
Insights
Congestive heart failure (CHF) involves maladaptive myocardial remodeling driven by matrix metalloproteinases (MMPs). Understanding how factors in CHF regulate MMPs offers potential therapeutic targets for heart failure.
Area of Science:
- Biochemistry
- Cardiovascular Biology
- Molecular Medicine
Background:
- Congestive heart failure (CHF) is characterized by maladaptive myocardial remodeling.
- This remodeling results from factors like myocardial infarction, hypertensive hypertrophy, and cardiomyopathy.
- Both cellular and extracellular components contribute to structural changes affecting cardiac function.
Purpose of the Study:
- To review the biology of matrix metalloproteinases (MMPs).
- To identify how biological factors active in CHF modulate the MMP family.
- To explore therapeutic interventions targeting MMP regulation in CHF.
Main Methods:
- Literature review focusing on MMPs in the context of CHF.
- Analysis of molecular mechanisms linking CHF-associated factors to MMP induction.
- Discussion of upstream molecules involved in MMP regulation.
Main Results:
- Matrix metalloproteinases (MMPs) are key enzymes in myocardial remodeling associated with CHF.
- Bioactive molecules (cytokines, neurohormones) and transcription factors in CHF induce MMPs.
- Extracellular stimuli in CHF contribute to MMP dysregulation.
Conclusions:
- MMPs play a critical role in the maladaptive remodeling underlying CHF.
- Understanding the regulation of MMPs by CHF-specific factors is crucial.
- Targeting upstream regulators of MMPs presents a promising therapeutic strategy for CHF.
Abstract:
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.
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