Oxidized LDL and HDL: antagonists in atherothrombosis

Mertens, Ann; Holvoet, Paul

doi:10.1096/fj.01-0273rev

Cited by 364 publications

(276 citation statements)

References 138 publications

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“…Oxidized LDL generated by oxidative stress also promotes the progression of arteriosclerosis. [27][28][29] In this study, plasma HSCRP and MDA-LDL levels were lower with azelnidipine than with thiazide therapy. The antioxidant effect of azelnidipine possibly participated in the reduction of plasma MDA-LDL levels.…”

Section: Combined Antihypertensive Therapy With Olmesartan T Ishimitsmentioning

confidence: 60%

Angiotensin-II receptor antagonist combined with calcium channel blocker or diuretic for essential hypertension

et al. 2009

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To achieve the target blood pressure recommended by the latest guidelines, multiple antihypertensive drugs are needed in most patients. In this study, the efficacy of treatment using an angiotensin II receptor antagonist (ARB) combined with a calcium channel blocker (CCB) or a diuretic was compared from multiple perspectives in patients with hypertension. Twenty-nine patients with essential hypertension, who had failed to achieve their target blood pressure (o130/85 mm Hg for patients o65 years old and o140/90 mm Hg for those X65 years) when treated with the ARB olmesartan at 20 mg day À1 , were additionally given 8-16 mg day À1 of the CCB azelnidipine or 1-2 mg day À1 of trichlormethiazide (a thiazide diuretic) in a randomized crossover manner for 4 months each. At the end of each combination therapy period, blood and urine samples were collected and arterial stiffness was evaluated by measuring the cardio-ankle pulse wave velocity. Compared with monotherapy, the blood pressure was reduced similarly by adding azelnidipine (À12/À10 mm Hg) or trichlormethiazide (À14/À9 mm Hg). The heart rate was decreased with the CCB by 4 b.p.m. (Po0.05), whereas it was unchanged with the thiazide. Serum K, lipids and blood glucose were not significantly changed with either combination, whereas serum uric acid was increased with the thiazide (Po0.01) but was unchanged with azelnidipine. Plasma levels of renin, angiotensin II and aldosterone were also increased with the thiazide period, whereas high-sensitivity C-reactive protein and oxidized low-density lipoprotein were decreased with azelnidipine. In addition, the cardio-ankle vascular index, a parameter of arterial stiffness, was decreased with the azelnidipine period but was unchanged with the thiazide period (Po0.01). It is suggested that the combination of olmesartan and azelnidipine has advantages over the combination of olmesartan and a thiazide with respect to avoiding hyperuricemia, sympathetic activation, renin-angiotensin-aldosterone system stimulation, inflammation, oxidative stress, and increased arterial stiffness in patients with moderate hypertension. These properties may provide cardiovascular protection in addition to the hypotensive effect.

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Section: Combined Antihypertensive Therapy With Olmesartan T Ishimitsmentioning

confidence: 60%

Angiotensin-II receptor antagonist combined with calcium channel blocker or diuretic for essential hypertension

et al. 2009

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“…Indeed, ox-LDL was found to induce metalloproteases, which degrade matrix proteins, important for SMC migration, and, in addition, ox-LDL induces SMC apoptosis. 36 It has been shown that Pparg exerts anti-inflammatory actions by antagonizing the transcriptional activity of Nfkb1. 37 Accordingly, stevioside-treated mice showed a lower Nfkb1/Nfkbia ratio.…”

Section: Discussionmentioning

confidence: 99%

Stevioside inhibits atherosclerosis by improving insulin signaling and antioxidant defense in obese insulin-resistant mice

et al. 2009

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Objective: Stevioside is a non-caloric natural sweetener that does not induce a glycemic response, making it attractive as sweetener to diabetics and others on carbohydrate-controlled diets. Obesity is frequently associated with insulin resistance and increased inflammation and oxidative stress. Therefore, we investigated its effects on insulin resistance, inflammation and oxidative stress related to atherosclerosis in obese insulin-resistant mice.Research design: Twelve-week-old mice were treated with stevioside (10 mg kg À1 , n ¼ 14) or placebo (n ¼ 20) for 12 weeks. Results: Stevioside had no effect on weight and triglycerides, but lowered glucose and insulin. Stevioside treatment improved adipose tissue maturation, and increased glucose transport, insulin signaling and antioxidant defense in white visceral adipose tissues. Together, these increases were associated with a twofold increase of adiponectin. In addition, stevioside reduced plaque volume in the aortic arch by decreasing the macrophage, lipid and oxidized low-density lipoprotein (ox-LDL) content of the plaque. The higher smooth muscle cell-to-macrophage ratio was indicative for a more stable plaque phenotype. The decrease in ox-LDL in the plaque was likely due to an increase in the antioxidant defense in the vascular wall, as evidenced by increased Sod1, Sod2 and Sod3. Circulating adiponectin was associated with improved insulin signaling and antioxidant defense in both the adipose tissue and the aorta of stevioside-treated mice. Conclusion: Stevioside treatment was associated with improved insulin signaling and antioxidant defense in both the adipose tissue and the vascular wall, leading to inhibition of atherosclerotic plaque development and inducing plaque stabilization.

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“…Atherosclerosis has been documented as an inflammatory disease and is associated with increased O 2 ·-and other ROS (Griendling et al 2000b;Patel et al 2000a;Patel et al 2000b;Mertens et al 2001;Harrison et al 2003b;Lassegue et al 2003;Wassmann et al 2004). Possible signaling mechanisms for the inflammatory based reaction are discussed in section 2.3.…”

Section: Atherosclerosismentioning

confidence: 99%

“…It may play a role in the oxidation of LDL and formation of lipid free radicals, which are capable of scavenging NO (Parthasarathy et al 1989;Mertens et al 2001). Lipoxygenase is also thought to contribute to angiotensin II activation of NADPH oxidase O 2 ·-formation during cardiovascular disease (Luchtefeld et al 2003).…”

Section: Lipoxygenasementioning

confidence: 99%