The selective peroxisomal proliferator-activated receptor-gamma agonist has an additive effect on plaque regression in combination with simvastatin in experimental atherosclerosis

Corti, Roberto; Osende, Julio I.; Fallon, John T.; Fuster, Valentín; Mizsei, Gabor; Jneid, Hani; Wright, Samuel D.; Chaplin, William F.; Badimón, Juan J.

doi:10.1016/j.jacc.2003.08.048

Cited by 95 publications

(65 citation statements)

References 45 publications

(47 reference statements)

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“…Statins are reported to activate PPAR-γ and inhibit LPS-induced cytokine expression in macrophages [21]. These findings are supported by data demonstrating that statins stabilize atherosclerotic plaques through the activation of PPAR-γ and that combined administration of simvastatin with PPAR-γ agonists elicits additive effects on atherosclerotic plaque regression [22][23][24].…”

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confidence: 82%

The Pleiotropic Effects of Statins in the Prevention of Atherosclerosis

Kong

Zhu

2011

Cardiovasc Drugs Ther

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confidence: 82%

The Pleiotropic Effects of Statins in the Prevention of Atherosclerosis

Kong

Zhu

2011

Cardiovasc Drugs Ther

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“…One month postoperatively, aortic atherosclerotic lesions were induced by 9 months of 0.2% cholesterolenriched rabbit diet (WIL Research Laboratories; Ashland, Ohio) and double ballooninduced aortic endothelial denudation as previously described. [18][19][20][21][22][23] All procedures were performed under general anesthesia by intramuscular injection of acepromazine (1 mg/kg; Boehringer Ingelheim Vetmedica; St. Joseph, Missouri), ketamine (20 mg/kg; Fort Dodge Animal Health; Fort Dodge, Iowa), and xylazine (2 mg/kg; Lloyd Laboratories; Shenandoah, Iowa). This experimental model of atherosclerosis has reliably demonstrated reproducible development of advanced atherosclerotic lesions, [18][19][20][21][22][23] and the study protocol was approved by the Institutional Animal Care and Use Committee of the Mount Sinai School of Medicine.…”

Section: Experimental Model Of Atherosclerosismentioning

confidence: 99%

“…19 The acquired MRIs were transferred to a Macintosh computer system (Apple; Cupertino, California) for analysis. The pre-and post-treatment images were matched for anatomic position by using distances from the renal arteries and iliac bifurcation as previously validated, 19 so that each animal served as its own control and true serial data on atherosclerotic progression/regression could be obtained. The 6 cm of aorta immediately distal to the left renal artery, corresponding to 20 contiguous MRI segments, were selected for vessel wall measurements.…”

Section: In Vivo Magnetic Resonance Imaging Of Atherosclerotic Lesionsmentioning

confidence: 99%

mentioning

confidence: 99%

“…The sample size was calculated to detect change in aortic vessel wall area as assessed by serial MRI (the pre-specified primary endpoint) based upon a power of 0.8 and α of 0.05, observations from a prior experimental model of raloxifene administration, and measurement error from prior MRI studies in our laboratory using the same experimental model. 9,[18][19][20][21][22][23] Observers for all measurements (MRI, histopathology, Western blot, platelet aggregometry and μCT) were blinded to treatment group. …”

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Selective estrogen receptor modulation influences atherosclerotic plaque composition in a rabbit menopause model

et al. 2008

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Objective-Osteoporosis trials suggest raloxifene decreased cardiovascular events in women with preexisting atherosclerosis. We assessed the hypothesis that selective estrogen receptor modulation induces plaque stability in "menopausal" animals.Methods and Results-Atherosclerosis was induced in 42 ovariectomized New Zealand White rabbits by cholesterol feeding and mechanical injury. Animals were imaged by magnetic resonance (MRI) for baseline atherosclerosis, and randomized to control (OVX, n=12), raloxifene 35-60 mg/kg/day by diet admixture (RLX, n=24), or immediate sacrifice (n=6) for immunohistopathologic correlation of MRI. Six months later, rabbits underwent repeat MRI then sacrifice for micro-computed tomography (μCT) and molecular analysis. Unlike OVX, RLX reduced atheroma volume. Analysis for lesion inflammation revealed reductions in COX-2, MMP-1, MCP-1 expression and macrophage infiltration in RLX vs. OVX with concomitant upregulation of estrogen receptor α. μCT showed similar total vascular calcification between groups, but calcifications in RLX were less nodular with better radial organization (mean calcific arc angle 63 ± 7° vs. 33 ± 6° in OVX), the predicted result of a 53% increase in BMP-2. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. Conclusions-Raloxifene NIH Public Access Author ManuscriptAtherosclerosis. Author manuscript; available in PMC 2012 July 02. Recent efforts at female-specific pharmacologic therapies have focused on selective estrogen receptor modulators (SERMs). Most pertinently, post-hoc analysis from an osteoporosis treatment trial in post-menopausal women (the Multiple Outcomes of Raloxifene Evaluation, MORE) found that those women at high-risk for coronary artery disease (i.e., a secondary prevention population most likely to have established atherosclerotic lesions) treated with the SERM raloxifene had 40 percent fewer cardiovascular events than those on placebo. 5 The Raloxifene Use for the Heart (RUTH) study, which was a double-blind, placebo-controlled, randomized clinical trial of this SERM's use in a patient population without pre-specified osteoporosis did not confirm this benefit. 6, 7The mechanism of raloxifene's potential effects upon atherosclerotic lesions is not completely understood. Pre-clinical animal models have shown that raloxifene, similar to HT, inhibits atherosclerosis, 8, 9 but its effect upon vascular calcification is unknown. HT results in less calcified plaques 10 without clear reduction in cardiovascular events, 11 yet statins, a therapy with clear reductions in cardiovascular events, increase calcifi...

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Atherosclerotic Plaque Imaging

et al. 2005

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Coronary artery disease imaging has traditionally been based on luminal angiography, but it has become evident that this tool, although extremely useful in diagnosing obstructive disease, is insufficient to define the presence and extent of atherosclerotic disease in the vessel wall. Progression of coronary artery disease was also initially evaluated using quantitative coronary angiography, and evidence soon accumulated that minor regression or nonprogression of luminal disease was associated with a favorable cardiovascular outcome. In recent years, however, several other techniques have been developed to image atherosclerosis and are emerging as useful tools in preventive cardiovascular medicine. These techniques provide new methods to assess the burden of atherosclerosis, gauge the risk of cardiovascular events, and offer a means to test the efficacy of therapeutic approaches to atherosclerosis. Furthermore, noninvasive coronary angiography can be performed with some of the new imaging modalities, potentially reducing the number of unnecessary invasive tests. This review focuses on techniques such as cardiac computed tomography, carotid artery intima-media thickness, cardiovascular magnetic resonance imaging, and intravascular ultrasonography as emerging tools in cardiovascular disease prevention.

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The selective peroxisomal proliferator-activated receptor-gamma agonist has an additive effect on plaque regression in combination with simvastatin in experimental atherosclerosis

Cited by 95 publications

References 45 publications

The Pleiotropic Effects of Statins in the Prevention of Atherosclerosis

The Pleiotropic Effects of Statins in the Prevention of Atherosclerosis

Selective estrogen receptor modulation influences atherosclerotic plaque composition in a rabbit menopause model

Atherosclerotic Plaque Imaging

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