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Rosuvastatin inhibits TIMP-2 and promotes myocardial angiogenesis

Anwar J Siddiqui1, Thomas Gustafsson, Christer Sylven

  • 1Department of Laboratory Medicine, Care Sciences and Society (Clinical Geriatrics), Karolinska University Hospital Huddinge and Karolinska Institute, Stockholm, Sweden.

Pharmacology
|May 24, 2014
PubMed
Abstract

Insights

Rosuvastatin (RSV) treatment in mice altered expression of tissue inhibitors of metalloproteinases (TIMPs), vascular endothelial growth factor-A (VEGF-A), and estrogen receptor-α (ER-α), potentially promoting arteriolar growth in the myocardium.

Area of Science:

  • Cardiovascular Research
  • Molecular Biology
  • Pharmacology

Background:

  • Angiogenesis, the formation of new blood vessels, is often linked to inflammation.
  • Matrix metalloproteinases (MMPs) and their inhibitors (TIMPs) play roles in vascular remodeling.
  • Statins, beyond lipid-lowering, possess both pro- and antiangiogenic properties.

Purpose of the Study:

  • To investigate the effects of rosuvastatin (RSV) on myocardial vascular remodeling in ApoE knockout mice.
  • To examine the expression of MMP-3, MMP-9, TIMP-1, TIMP-2, VEGF-A, and ER-α in response to RSV treatment.

Main Methods:

  • ApoE knockout mice were fed a high-cholesterol diet with or without rosuvastatin (RSV).
  • Hearts were analyzed for mRNA expression of MMP-3, MMP-9, TIMP-1, TIMP-2, VEGF-A, and ER-α.

Main Results:

  • RSV significantly inhibited TIMP-1 and TIMP-2 expression.
  • RSV enhanced myocardial VEGF-A and ER-α expression, independent of lipid levels.
  • RSV did not affect MMP-3 and MMP-9 expression.

Conclusions:

  • RSV-induced modulations in TIMPs, VEGF-A, and ER-α may stimulate arteriolar growth in the myocardium.
  • These findings suggest a potential role for statins in promoting myocardial vascularization through non-lipid-lowering mechanisms.

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