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Updated: Apr 3, 2026

Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice
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Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice

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Pitavastatin Reduces Inflammation in Atherosclerotic Plaques in Apolipoprotein E-Deficient Mice with Late Stage Renal

Manabu Shibasaki1, Jian-Guo Wang1, Jose-Luiz Figueiredo1

  • 1Center for Interdisciplinary Cardiovascular Sciences (CICS), Division of Cardiovascular Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, 02115, United States of America.

Plos One
|September 15, 2015
PubMed

Insights

Pitavastatin significantly reduced arterial inflammation and stenosis in mice with chronic renal disease (CRD). While it lowered macrophage accumulation and osteopontin levels, pitavastatin did not significantly reduce arterial calcification in CRD mice.

Area of Science:

  • Cardiovascular Research
  • Nephrology
  • Pharmacology

Background:

  • Chronic renal disease (CRD) accelerates atherosclerosis and cardiovascular calcification.
  • Statins are used to lower cholesterol, but their cardiovascular benefits in CRD patients are not fully understood.
  • Pitavastatin is a novel statin with potential therapeutic effects.

Purpose of the Study:

  • To investigate the effects of pitavastatin on arterial inflammation and calcification in a mouse model of CRD.
  • To assess pitavastatin's impact on macrophage accumulation and key molecular markers in atherosclerosis.

Main Methods:

  • CRD was induced in apolipoprotein E-deficient mice via 5/6 nephrectomy.
  • Mice were divided into control, CRD, and pitavastatin-treated CRD groups.
  • Ultrasonography, near-infrared molecular imaging, Mac3 immunostaining, and histology were used to evaluate arterial changes.

Main Results:

  • Pitavastatin significantly reduced brachiocephalic artery stenosis and macrophage accumulation in CRD mice.
  • Osteopontin levels in plasma and atherosclerotic lesions were reduced by pitavastatin.
  • Pitavastatin did not significantly reduce calcification in atherosclerotic plaques, and plasma phosphate levels remained unchanged.

Conclusions:

  • Pitavastatin demonstrates in vivo efficacy in reducing inflammation within atherosclerotic lesions in CRD mice.
  • The findings suggest pitavastatin may have anti-inflammatory benefits in the context of CRD-associated atherosclerosis.
Abstract

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