Molecular Mechanisms of HDL-Cholesterol Elevation by Statins and Its Effects on HDL Functions

Yamashita, Shizuya; Tsubakio-Yamamoto, Kazumi; Ohama, Tohru; Nakagawa-Toyama, Yumiko; Nishida, Makoto

doi:10.5551/jat.5405

Cited by 84 publications

(61 citation statements)

References 146 publications

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“…Furthermore, many studies have documented that the protective nature of HDL-C can be altered in the presence of glucose intolerance or diabetes and under conditions of inflammation where HDL-C can be modified by oxidative processes and replacement or modification of its protein and lipid components 41) . Surprisingly, in our patients, LDL-C concentration was not associated with cardiac events during follow-up, probably due to the effects of pharmacological treatment, mainly statins, which reduce LDL-C levels but have little effect on HDL-C levels, differing according to the types and doses of statins 42) . Regarding low HDL-C concentrations, we found values ＜35 mg/dL to be more closely associated with cardiac events than those below the more commonly accepted cut-off value of ＜40 mg/dL.…”

Section: Follow-upmentioning

confidence: 96%

High Density Lipoprotein Cholesterol in Coronary Artery Disease: When Higher Means Later

Sbrana

Puntoni

Bigazzi

et al. 2013

JAT

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Aim: Although high-density lipoprotein cholesterol (HDL-C) levels are inversely associated with cardiovascular risk, patients with elevated HDL-C also develop coronary artery disease (CAD) and cardiac events. We aimed to draw the clinical profile of CAD patients with elevated HDL-C and to assess the prognostic impact of elevated HDL-C. Methods: We prospectively examined 2322 patients (age 67±10 years, 79% male) with chronic CAD, defined by ＞50% coronary stenosis and/or previous myocardial infarction.

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Section: Follow-upmentioning

confidence: 96%

High Density Lipoprotein Cholesterol in Coronary Artery Disease: When Higher Means Later

Sbrana

Puntoni

Bigazzi

et al. 2013

JAT

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“…Atorvastatin has a positive impact on plasma total antioxidant status and PON1 activity by reducing plasma susceptibility to lipid peroxidation induced by free radicals (Fuhrman et al 2002;Harangi et al 2004Harangi et al , 2009Nagila et al 2009). Pitavastatin was also shown to increase the promoter activity and protein expression of PON1 in vitro via p44/42 mitogen-activated protein kinase-mediated phosphorylation of sterol-regulatory-element-binding protein-2 and binding of Sp1 to PON1 DNA (Arii et al 2009;Yamashita et al 2010). The improvement of antioxidant properties of HDL, via increased PON1 activity, was also observed after simvastatin and fluvastatin therapy (Bergheanu et al 2007;Mirdamadi et al 2008;Muacevic-Katanec et al 2007).…”

Section: Statinsmentioning

confidence: 99%

Effects of Established Hypolipidemic Drugs on HDL Concentration, Subclass Distribution, and Function

Gomaraschi

Adorni

Banach

et al. 2014

High Density Lipoproteins

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“…A low level of HDL-C increases the risk for CHD and increases mortality. 19) However, some evidences weaken the hypotheses that HDL-C level relate directly to CHD status and that elevating HDL-C is necessary. 20) in our study, we found 3,4-DHAP could decrease the plasma HDL-C level, but 3,4-DHAP exhibits an anti-atherosclerotic effect.…”

Section: )mentioning

confidence: 99%

Effects of 3,4-Dihydroxyacetophenone on the Hypercholesterolemia-Induced Atherosclerotic Rabbits

Zhang

Liu

Wang

et al. 2013

Biological & Pharmaceutical Bulletin

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3,4-Dihydroxyacetophenone (3,4-DHAP) is one herbal extract from bald Mao-dong-qing leaves. We reported that 3,4-DHAP had anti-inflammatory function by decreasing tumor necrosis factor-α (TNF-α) secretion in macrophages. The aim of the study was to examine the effects of 3,4-DHAP on plasma and liver lipids, plasma alanine aminotranferase (ALT) and TNF-α level, vascular cell adhesion molecule-1 (VCAM-1) expression, plaque vulnerability and vascular inflammation in hypercholesterolemia-induced atherosclerotic rabbits. Male New Zealand white rabbits were randomized into negative control, positive control, 3,4-DHAP and simvastatin groups. From weeks 2 to 12, the rabbits were treated with 3,4-DHAP or simvastatin. At weeks 12, all the animals were sacrificed. Plasma lipids and ALT were measured using the enzymatic endpoint method. Plasma TNF-α was measured using enzyme-linked immuno sorbent assay (ELISA). Liver lipids concentrations were estimated using commercial kits. The expression of VCAM-1 was measured using reverse transcription-polymerase chain reaction (RT-PCR) and Western blot. Histological analysis was used to evaluate the pathologic changes of rabbit aortas. The results showed that 3,4-DHAP markedly lowered plasma and liver lipids, lowered plasma ALT and TNF-α levels compared with the positive control group. VCAM-1 mRNA and protein were markedly inhibited by 3,4-DHAP. Decreased aortic plaque instability was evident in 3,4-DHAP-treated rabbits, as demonstrated by a thickened elastic layer, increased vascular smooth muscle cells (VSMCs) accumulation in the plaques, less neointima hyperplasia and macrophages recruitment. 3,4-DHAP may attenuate the progression of atherosclerotic lesions and stabilize plaques by lowering plasma lipids, the number of macrophages and the expression of VCAM-1, while increasing the number of VSMCs in the atherosclerotic plaques. Key words 3,4-dihydroxyacetophenone; vascular cell adhesion molecule-1; atherosclerosisAtherosclerosis is an inflammatory disease.1) Atherosclerosis associated with the rupture of vulnerable plaque is the main cause of cardiovascular events. The characteristics of vulnerable plaque include a large lipid core, thin fibrous cap, inflammation and immune cell activation.2) Growing evidence shows that macrophages play a pivotal role in all stages of atherosclerosis. Vascular cell adhesion molecule-1 (VCAM-1) can strength the adhesion of leukocytes to vascular wall, promote leukocytes entering intima, transforming into macrophages. 3)Evidence is accumulating that low-density lipoprotein cholesterol (LDL-C) is the principal risk factor for atherosclerosis, and it is identified as the primary target for cholesterol-lowering therapy.4) Tumor necrosis factor-α (TNF-α) is one of the most important mediators of inflammation and may mediate endothelial dysfunction. 5,6)3,4-Dihydroxyacetophenone (3,4-DHAP) is extracted from herb; clinical experiments and pharmacological studies of it have been on for many years in coronary heart disease, pregnancy-induced hypertension synd...

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Molecular Mechanisms of HDL-Cholesterol Elevation by Statins and Its Effects on HDL Functions

Cited by 84 publications

References 146 publications

High Density Lipoprotein Cholesterol in Coronary Artery Disease: When Higher Means Later

High Density Lipoprotein Cholesterol in Coronary Artery Disease: When Higher Means Later

Effects of Established Hypolipidemic Drugs on HDL Concentration, Subclass Distribution, and Function

Effects of 3,4-Dihydroxyacetophenone on the Hypercholesterolemia-Induced Atherosclerotic Rabbits

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