Inflammation, Atherosclerosis, and Coronary Artery Disease

Kriszbacher, I; Koppán, Miklós; Bódis, József

doi:10.1056/nejm200507283530425

Cited by 141 publications

(31 citation statements)

References 14 publications

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“…Inflammation plays an important role in the pathogenesis of vascular endothelial injury [35,36]. Endothelial dysfunction leads to atherosclerosis and restenosis by facilitating platelet adhesion and aggregation and by signaling the release of mitogens from platelets, macrophages, and endothelial cells, which stimulate smooth muscle cell proliferation [37].…”

Section: Discussionmentioning

confidence: 99%

Anti-Inflammatory Effects of Tanshinone IIA on Atherosclerostic Vessels of Ovariectomized ApoE-/- Mice are Mediated by Estrogen Receptor Activation and Through the ERK Signaling Pathway

Liu¹,

Guo²,

Ma³

et al. 2015

Cell Physiol Biochem

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Aims: Estrogen plays a protective role in atherosclerosis. Our preliminary work demonstrated that the active conformation of Tanshinone IIA(TanIIA) is similar to the 17ß-estradiol and it can bind to the estrogen receptor. Here, we hypothesized that Tanshinone IIA might have anti-inflammatory and anti-oxidative effects in atherosclerosis, mediated through estrogen receptor activation. Methods: Subjects for this study were 120 apoE^-/- female mice and 20 C57/BL female mice. The apoE^-/- mice were ovariectomized (OVX) and the C57/BL mice were sham ovariectomized. The sham OVX mice were maintained on a normal diet (NOR) group. The OVX apoE^-/- mice were fed a high fat diet and randomly divided into 6 groups: Model (MOD) group which was fed a high fat diet only, E₂ group were given estrogen (E₂) 0.13mg/kg/d; E₂+ICI group were given E₂:0.13mg/kg/d and ICI182780:65mg/kg/m; TLD group (TanIIA low dose) were given TanIIA: 30mg/kg/d; THD group (TanIIA high dose) were given TanIIA:60mg/kg/d; and TLD+ICI group were given TanIIA 30mg/kg/d and ICI182780 65mg/kg/m. After three months of treatment, the aorta and the blood of the mice from each group was collected. The aorta were used for testing the lipid deposition by using hematoxylin and eosin(HE) and oil red O staining and for testing the expression of p-ERK1/2 by Western blot. The blood was used for testing the serum cholesterol, superoxide dismutase (SOD), methane dicarboxylic aldehyde (MDA), nuclear factor kappa (NF-κB), soluble intercellular cell adhesion molecule-1 (sICAM-1), activating protein-1 (AP-1), E-selectin and 17ß-estradiol in serum. Results: Tanshinone IIA significantly reduced the lipid deposition in aorta, decreased the levels of total cholesterol (TC), triglyceride (TG), low density lipoprotein (LDL), very low density lipoprotein (VLDL), MDA, NF-κB, sICAM-1, AP-1, and E-selectin in serum but increased the levels of high density lipoprotein (HDL) and SOD in serum. Tanshinone IIA also suppressed the expression of p-ERK1/2. Tanshinone IIA had no effect of level of serum 17ß-estradiol levels. All of the effects of Tanshinone IIA were similar to estrogen and were inhibited by the estrogen receptor antagonist ICI182780. Conclusion: Tanshinone IIA may play an anti-inflammatory and anti-oxidative stress role in OVX atherosclerotic apoE^-/- mice by activating the estrogen receptor through the ERK signaling pathway. Therefore, Tanshinone IIA, as a phytoestrogen, could be used for estrogen replacement therapy for cardiovascular disease of postmenopausal women.

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Section: Discussionmentioning

confidence: 99%

Anti-Inflammatory Effects of Tanshinone IIA on Atherosclerostic Vessels of Ovariectomized ApoE-/- Mice are Mediated by Estrogen Receptor Activation and Through the ERK Signaling Pathway

Liu¹,

Guo²,

Ma³

et al. 2015

Cell Physiol Biochem

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“…Is it merely an accompanying phenomenon or is there specific clinical significance? In studies involving patients and animals with atherosclerosis in which the pathogenic effect of FCs has been demonstrated, FC secretes soluble interleukin-1, tumor necrosis factor-α, and macrophage chemokine-1 (MCP-1), thus promoting a local inflammatory reaction and facilitating the development of atherosclerosis [15,16,17,18]. Thus, the presence of FCs in atherosclerotic plaques is not only the passive outcome of lipid endocytosis, but may also play an active role in disease progression.…”

Section: Discussionmentioning

confidence: 99%

Presence of Foam Cells in Kidney Interstitium Is Associated with Progression of Renal Injury in Patients with Glomerular Diseases

Chen²,

Chen³

et al. 2009

Nephron Clin Pract

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Background: Renal interstitial foam cells (FCs) are occasionally observed in various renal diseases. The goal of the present study was to determine the relationship between the formation of renal interstitial FCs and the degree of proteinuria and hyperlipidemia, as well as the progression of these diseases. Methods: 125 patients with Alport syndrome (AS), 192 patients with idiopathic membranous nephropathy (IMN), 388 patients with IgA nephropathy (IgAN), and 137 patients with focal segmental glomerulosclerosis (FSGS) were investigated retrospectively. Results: FCs were observed in various glomerular diseases. The frequency of interstitial FCs was 64.8% in AS, 21.4% in MN, 12.4% in IgAN, and 36.5% in FSGS. Regardless of the pathologic diagnosis of the glomerular disease, segmental glomerular sclerosis occurred more frequently in patients with FCs than in patients without FCs. In the AS or IgAN group, interstitial fibrosis was more severe, and levels of proteinuria and serum lipids were significantly higher in FC-positive patients than in patients without FCs. Conclusion: FC formation in renal interstitium is associated with the degree of proteinuria and hyperlipidemia in patients with AS and IgAN. The presence of FCs in renal interstitium may contribute to the progression of glomerular diseases.

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“…Inflammation plays an important role in the development of AS [39-41]. Monocytes release a large number of inflammatory cytokines, such as IL-1, IL-6 and TNF-α, which contribute to vascular endothelium injury and induce the formation of plaque [42-44].…”

Section: Discussionmentioning

confidence: 99%

The Influence of Hyperlipidemia on Endothelial Function of FPN1 Tek-Cre Mice and the Intervention Effect of Tetramethylpyrazine

Sun

Zhang

Chen

et al. 2018

Cell Physiol Biochem

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Background/Aims: Systemic iron homeostasis is strictly governed in mammals; however, disordered iron metabolism (such as excess iron burden) is recognized as a risk factor for various types of diseases including AS (Atherosclerosis). The hepcidin-ferroportin axis plays the key role in regulation of iron homeostasis and modulation of this signaling could be a potential therapeutic strategy in the treatment of these diseases. TMP (Tetramethylpyrazine) has been reported to have therapeutical effect on AS. Here, we aimed to investigate the effect of iron overload under hyperlipidemia condition on the endothelial injury, inflammation and oxidative stress by employing FPN1 Tek-cre mouse model with or without TMP intervention. Methods: Subjects for this study were 80 FPN1 Tek-cre mice and 40 C57BL/6 mice and we randomly divided them into six groups: Group N: C57BL/6 mice with normal diet, Group M: C57BL/6 mice with high-fat diet, Group FN: FPN1 Tek-cre mice with normal diet, Group FNT: FPN1 Tek-cre mice with normal diet and TMP injection, Group FM: FPN1 Tek-cre mice with high-fat diet, Group FMT: FPN1 Tek-cre mice with high-fat diet and TMP injection. After seven days of treatment, blood samples were obtained to detect the levels of blood lipids, Hepcidin, NO, ET-1, ROS, MDA, SOD, IL-1, IL-6 and TNF-α respectively. The liver and aorta were used for testing the lipid deposition by using hematoxylin and eosin(HE). Results: Hyperlipidemia could cause iron overload in the aorta and increased serum hepcidin level, particularly in FPN1 Tek-cre mice, and can be reversed by TMP intervention. Knockout of Fpn1 induced increase of serum hepcidin, exacerbated endothelial dysfunction, oxidative stress and inflammatory response, particularly under hyperlipidemia condition. TMP intervention attenuated these processes. Conclusions: Our study signifies the potential application of certain natural compounds to ameliorating iron disorders induced by hyperlipidemia and protecting on endothelial function through modulation of hepcidin-ferroportin signaling.

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Inflammation, Atherosclerosis, and Coronary Artery Disease

Cited by 141 publications

References 14 publications

Anti-Inflammatory Effects of Tanshinone IIA on Atherosclerostic Vessels of Ovariectomized ApoE-/- Mice are Mediated by Estrogen Receptor Activation and Through the ERK Signaling Pathway

Anti-Inflammatory Effects of Tanshinone IIA on Atherosclerostic Vessels of Ovariectomized ApoE-/- Mice are Mediated by Estrogen Receptor Activation and Through the ERK Signaling Pathway

Presence of Foam Cells in Kidney Interstitium Is Associated with Progression of Renal Injury in Patients with Glomerular Diseases

The Influence of Hyperlipidemia on Endothelial Function of FPN1 Tek-Cre Mice and the Intervention Effect of Tetramethylpyrazine

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