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May 1, 2000Cardiovascular ResearchOpen Access

Myocardial matrix degradation and metalloproteinase activation in the failing heart: a potential therapeutic target

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Key result

Myocardial matrix metalloproteinase expression, including an over four-fold increase in MMP-3, contributes to left ventricular remodeling in dilated cardiomyopathy and represents a therapeutic target.

Why the study?

Does broad-spectrum pharmacological MMP inhibition attenuate left ventricular dilation and improve pump function in the setting of developing heart failure?

Population

Experimental and clinical forms of dilated cardiomyopathy, including ischemic and non-ischemic human DCM…

Design

Review

Authors

FSFrancis G. SpinaleHeart Failure & Transplant

Discussion

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Implication

MMP overexpression may promote remodeling in dilated cardiomyopathy; leaves open whether inhibition improves outcomes.

Structured PICO

Does broad-spectrum pharmacological MMP inhibition attenuate left ventricular dilation and improve pump function in the setting of developing heart failure?

P
Population
Experimental and clinical forms of dilated cardiomyopathy (DCM), including ischemic and non-ischemic human DCM, and a pacing model of left ventricular failure
I
Intervention
Broad-spectrum pharmacological matrix metalloproteinase (MMP) inhibitor
O
Outcome
Left ventricular dilation and left ventricular pump functionsurrogate

Increased myocardial matrix metalloproteinase expression and activity contribute to left ventricular remodeling in cardiomyopathy, highlighting MMP inhibition as a potential therapeutic target for heart failure.

Cite This Study

Francis G. Spinale (2000) conducted a review in Dilated cardiomyopathy and heart failure. Pharmacological MMP inhibitor was evaluated. Myocardial matrix metalloproteinase expression, including an over four-fold increase in MMP-3, contributes to left ventricular remodeling in dilated cardiomyopathy and represents a therapeutic target.

synapsesocial.com/papers/6a0f141c25c30b2cc7fa1719https://doi.org/10.1016/s0008-6363(99)00431-9

Topics

Heart failureHFrEF treatment
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Also Consider

Synapse has enriched 4 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Increase in cross-linking of type I and type III collagens associated with volume-overload hypertrophy.1988 · 125 citations
  2. 2Human 72-kilodalton type IV collagenase forms a complex with a tissue inhibitor of metalloproteases designated TIMP-2.1989 · 588 citations
  3. 3Mechanisms and Models in Heart Failure1999 · 778 citations
  4. 4Cytokine-stimulated human vascular smooth muscle cells synthesize a complement of enzymes required for extracellular matrix digestion.1994 · 647 citations