From endothelial dysfunction to atherosclerosis

Sitia, S.; Tomasoni, Livio; Atzeni, Fabiola; Ambrosio, Giuseppe; Cordiano, C; Catapano, Alberico L.; Tramontana, S; Perticone, Francesco; Naccarato, Paola; Camici, Paolo G.; Picaño, Eugenio; Cortigiani, Lauro; Bevilacqua, Maurizio; Milazzo, Laura; Cusi, Daniele; Barlassina, Cristina; Sarzi-Puttini, Piercarlo; Turiel, M.

doi:10.1016/j.autrev.2010.07.016

Cited by 469 publications

(336 citation statements)

References 35 publications

Supporting

Mentioning

319

Contrasting

Unclassified

Order By: Relevance

“…Reduced endothelial-dependent vasodilation of peripheral arteries contributes to the development of cardiovascular disease (CVD), [1][2][3] the leading cause of death in women. 4 Resting forearm blood flow (FBF) 5 and vasodilatory capacity 6 are decreased in overweight and obese adults.…”

Section: Introductionmentioning

confidence: 99%

“…As RET can improve brachial artery endothelial function in overweight/obese women, 9 RET may decrease AIx in this population. As endothelial dysfunction and increased AIx contribute to the development of CVD, [1][2][3]14 RET may have clinical benefits for preventing CVD in overweight/obese women. Therefore, the purpose of the present study was to evaluate the acute and chronic effects of resistance exercise on resting and post-exercise FBF, vasodilatory capacity and wave reflection in overweight and obese women.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Effects of resistance exercise training on resting and post-exercise forearm blood flow and wave reflection in overweight and obese women

Kingsley

Figueroa

2011

J Hum Hypertens

View full text Add to dashboard Cite

The vascular responses to acute resistance exercise and resistance exercise training (RET) in overweight women are unclear. Therefore, the purpose of this study was to examine the vasodilatory and wave reflection responses to acute resistance exercise before and after RET. In all, 24 overweight/obese (28.5 ± 0.6 kg m À2 ) women (44 ± 1 years of age) volunteered for this study. Forearm blood flow (FBF), vasodilatory capacity in response to reactive hyperemia (peak FBF) and wave reflection (radial tonometry) were measured, before and 15 min after five sets of leg press at 10-repetition maximum (RM). Measures of pulse wave reflection included the augmentation index (AIx) and the time of the reflected wave (Tr). Measurements were collected at baseline, after a 4-week control period (before RET) and after 12 weeks of whole-body RET using three sets of five exercises at 50-60% of 1-RM. There were no differences in vascular measurements at baseline or before RET for any variable. Resting FBF (66.7%) and peak FBF (51.6%) increased significantly (Po0.05) after RET compared with before RET. Postexercise FBF (48.9%) and peak FBF (41.1%) also increased significantly (Po0.05) after RET compared with before RET. Post-exercise AIx decreased significantly (Po0.05), whereas Tr increased significantly (Po0.05) compared with rest at all time points. However, AIx and Tr were unaltered by RET. The 12-week wholebody RET increased the resting and post-exercise FBF as well as vasodilatory capacity without changing wave reflection in premenopausal overweight women. RET may be an important non-pharmacological therapy for reducing cardiovascular risk in overweight and obese premenopausal women.

show abstract

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Effects of resistance exercise training on resting and post-exercise forearm blood flow and wave reflection in overweight and obese women

Kingsley

Figueroa

2011

J Hum Hypertens

View full text Add to dashboard Cite

show abstract

“…In addition, the interaction of AGEs with their receptor (RAGE) on the cell surface causes upregulation of transcription factors such as nuclear factor (NF)-jB, leading to the expression of various pro-inflammatory cytokines and cell adhesion molecules that cause increased recruitment of monocytes into endothelial cells (ECs). This implies that AGEs-RAGE interactions are key steps in EC dysfunction and atherosclerosis (Davignon & Ganz 2004;Sitia et al 2010;Mudau et al 2012). In the pathogenesis of vessel disease, the proliferation of vascular smooth muscle cells (VSMCs) is an important event in the progression and rupture of atherosclerotic plaque, which subsequently contributes to heart disease (Ross 1993).…”

Section: Introductionmentioning

confidence: 99%

Glycolaldehyde-derived advanced glycation end products (glycol-AGEs)-induced vascular smooth muscle cell dysfunction is regulated by the AGES-receptor (RAGE) axis in endothelium

Nam

Son

Lee

et al. 2015

Cell Communication & Adhesion

View full text Add to dashboard Cite

Advanced glycation end-products (AGEs) are involved in the development of vascular smooth muscle cell (VSMC) dysfunction and the progression of atherosclerosis. However, AGEs may indirectly affect VSMCs via AGEs-induced signal transduction between monocytes and human umbilical endothelial cells (HUVECs), rather than having a direct influence. This study was designed to elucidate the signaling pathway underlying AGEs-RAGE axis influence on VSMC dysfunction using a co-culture system with monocytes, HUVECs and VSMCs. AGEs stimulated production of reactive oxygen species and pro-inflammatory mediators such as tumor necrosis factor-a and interleukin1b via extracellular-signal-regulated kinases phosphorylation and nuclear factor-jB activation in HUVECs. It was observed that AGEs-induced pro-inflammatory cytokines increase VSMC proliferation, inflammation and vascular remodeling in the co-culture system. This result implies that RAGE plays a role in AGEs-induced VSMC dysfunction. We suggest that the regulation of signal transduction via the AGEs-RAGE axis in the endothelium can be a therapeutic target for preventing atherosclerosis.ARTICLE HISTORY

show abstract

“…Numerous studies have shown that the oxidative modification of oxLDL is extremely relevant in atherogenesis (32,33). oxLDL can be vigorously absorbed by macrophages via receptor-mediated endocytosis, which promotes foam cell formation (34).…”

Section: Discussionmentioning

confidence: 99%

Berberine combined with atorvastatin downregulates LOX-1 expression through the ET-1 receptor in monocyte/macrophages

Chi

et al. 2014

International Journal of Molecular Medicine

View full text Add to dashboard Cite

Abstract. Studies have shown that the oxidative modification of low-density lipoprotein (oxLDL) plays a major role in atherogenesis. Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) mediated the transport of oxLDL into macrophages, which promoted foam cell formation. Targeting LOX-1 may therefore be a promising approach to inhibit atherosclerosis. In the present study, we aimed to investigate the effect of berberine combined with atorvastatin on LOX-1 and explore the underlying molecular mechanism involved. Expression of LOX-1 in monocyte-derived macrophages (MDMs) exposed to berberine (0, 0.1, 1, 10 and 100 nM) and atorvastatin (100 nM) were analyzed by quantitative reverse transcription polymerase chain reaction (qRT-PCR) and western blot analysis. Results showed that the expression of LOX-1 was decreased in a dose-dependent manner. Additionally, knockdown of the endothelin-1 (ET-1) receptor significantly blocked the inhibitory effect of berberine on LOX-1 expression. Body weight (BW), liver weight (LW) and kidney weight (KW) in the model rats were markedly increased at concentrations of berberine ≥1 µmol/kg, while heart weight (HW) and spleen weight (SW) remained constant among all groups. Berberine combined with atorvastatin also decreased serum total cholesterol (TC), triglyceride (TG) and low-density lipoprotein-cholesterol (LDL-C) levels in the rat model as well as inflammation and oxidative stress. Furthermore, plasma ET-1 levels and LOX-1 expression were decreased by berberine combined with atorvastatin treatment, and the inhibitory effect on LOX-1 was impeded by an ET-1 receptor antagonist. The results demonstrated that berberine combined with atorvastatin downregulates LOX-1 expression through ET-1 receptors in monocyte/macrophages in vitro and in vivo.

show abstract

From endothelial dysfunction to atherosclerosis

Cited by 469 publications

References 35 publications

Effects of resistance exercise training on resting and post-exercise forearm blood flow and wave reflection in overweight and obese women

Effects of resistance exercise training on resting and post-exercise forearm blood flow and wave reflection in overweight and obese women

Glycolaldehyde-derived advanced glycation end products (glycol-AGEs)-induced vascular smooth muscle cell dysfunction is regulated by the AGES-receptor (RAGE) axis in endothelium

Berberine combined with atorvastatin downregulates LOX-1 expression through the ET-1 receptor in monocyte/macrophages

Contact Info

Product

Resources

About