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October 11, 2011Circulation103 citationsOpen Access

Lack of Tissue Inhibitor of Metalloproteinases 2 Leads to Exacerbated Left Ventricular Dysfunction and Adverse Extracellular Matrix Remodeling in Response to Biomechanical Stress

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VKVijay KandalamRBRatnadeep BasuLMLinn E. Moore

Structured PICO

P
Population
Preclinical model lacking Tissue Inhibitor of Metalloproteinases 2 (TIMP2) subjected to biomechanical stress/pressure overload
I
Intervention
Lack of TIMP2
O
Outcome
Left ventricular dysfunction and adverse extracellular matrix remodelingsurrogate

TIMP2 plays a critical role in preserving cardiac function and extracellular matrix integrity during biomechanical stress.

Abstract

Lack of TIMP2 leads to exacerbated cardiac dysfunction and remodeling after pressure overload because of excess activity of membrane type MMP and loss of integrin β1D, leading to nonuniform ECM remodeling and impaired myocyte-ECM interaction.

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Cite This Study

Kandalam et al. (2011) studied this question.

synapsesocial.com/papers/69d6cdf28dca315383ed90behttps://doi.org/10.1161/circulationaha.111.030338
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Differential Cardiac Remodeling in Preload Versus Afterload2010 · 315 citations
  2. 2Tissue Inhibitor of Matrix Metalloproteinase-1 in Norepinephrine-Induced Remodeling of the Mouse Heart2007 · 9 citations
  3. 3Myocardial Fibrosis in Severe Aortic Stenosis2010 · 2 citations
  4. 4Cardiac Restricted Overexpression of Membrane Type-1 Matrix Metalloproteinase Causes Adverse Myocardial Remodeling following Myocardial Infarction2010 · 65 citations
  5. 5Mice with Tissue Inhibitor of Metalloproteinases 4 (Timp4) Deletion Succumb to Induced Myocardial Infarction but Not to Cardiac Pressure Overload2010 · 92 citations