scholarly journals Estrogen protection, oxidized LDL, endothelial dysfunction and vasorelaxation in cardiovascular disease: New insights into a complex issue

2007 ◽  
Vol 73 (1) ◽  
pp. 6-7 ◽  
Author(s):  
C SUBAHPACKER
Keyword(s):  
Cardiovascular Disease ◽  
Endothelial Dysfunction ◽  
Oxidized Ldl ◽  
Complex Issue

Protective effects of soy-isoflavones in cardiovascular disease

2008 ◽  
Vol 28 (01/02) ◽  
pp. 85-88 ◽  
Author(s):  
D. Fuchs ◽  
H. Daniel ◽  
U. Wenzel
Keyword(s):  
Cardiovascular Disease ◽  
Endothelial Cells ◽  
Molecular Mechanisms ◽  
Dietary Intervention ◽  
Mononuclear Cells ◽  
Oxidized Ldl ◽  
Proteome Analysis ◽  
Soy Isoflavones ◽  
Protective Effects ◽  
Estrogen Production

SummaryEpidemiological studies indicate that the consumption of soy-containing food may prevent or slow-down the development of cardiovascular disease. In endothelial cells application of a soy extract or a combination of the most abundant soy isoflavones genistein and daidzein both inhibited apoptosis, a driving force in atherosclerosis development, when applied in combination with oxidized LDL or homocysteine. Proteome analysis revealed that the stressorinduced alteration of protein expression profile was reversed by the soy extract or the genistein/daidzein mixture. Only few protein entities that could be functionally linked to mitochondrial dysfunction were regulated in common by both application forms of isoflavones. A dietary intervention with isoflavone-enriched soy extract in postmenopausal women, who generally show strongly increased cardiovascular risk due to diminished estrogen production, led to significant alterations in the steady state levels of proteins from mononuclear blood cells. The proteins identified by proteome analysis revealed that soy isoflavones may increase the anti-inflammatory response in blood mononuclear cells thereby contributing to the atherosclerosispreventive activities of a soy-rich diet. Conclusion: By proteome analysis protein targets were identified in vitro in endothelial cells that respond to soy isoflavones and that may decipher molecular mechanisms through which soy products exert their protective effects in the vasculature.

scholarly journals Endothelial Dysfunction, Atherosclerosis, and Increase of von Willebrand Factor and Factor VIII: A Randomized Controlled Trial in Swine

2021 ◽  
Author(s):  
Ferdows Atiq ◽  
Jens van de Wouw ◽  
Oana Sorop ◽  
Ilkka Heinonen ◽  
Moniek P. M. de Maat ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Randomized Controlled Trial ◽  
Endothelial Dysfunction ◽  
Controlled Trial ◽  
Short Term ◽  
Randomized Controlled ◽  
Von Willebrand ◽  
Willebrand Factor

AbstractIt is well known that high von Willebrand factor (VWF) and factor VIII (FVIII) levels are associated with an increased risk of cardiovascular disease. It is still debated whether VWF and FVIII are biomarkers of endothelial dysfunction and atherosclerosis or whether they have a direct causative role. Therefore, we aimed to unravel the pathophysiological pathways of increased VWF and FVIII levels associated with cardiovascular risk factors. First, we performed a randomized controlled trial in 34 Göttingen miniswine. Diabetes mellitus (DM) was induced with streptozotocin and hypercholesterolemia (HC) via a high-fat diet in 18 swine (DM + HC), while 16 healthy swine served as controls. After 5 months of follow-up, FVIII activity (FVIII:C) was significantly higher in DM + HC swine (5.85 IU/mL [5.00–6.81]) compared with controls (4.57 [3.76–5.40], p = 0.010), whereas VWF antigen (VWF:Ag) was similar (respectively 0.34 IU/mL [0.28–0.39] vs. 0.34 [0.31–0.38], p = 0.644). DM + HC swine had no endothelial dysfunction or atherosclerosis during this short-term follow-up. Subsequently, we performed a long-term (15 months) longitudinal cohort study in 10 Landrace–Yorkshire swine, in five of which HC and in five combined DM + HC were induced. VWF:Ag was higher at 15 months compared with 9 months in HC (0.37 [0.32–0.42] vs. 0.27 [0.23–0.40], p = 0.042) and DM + HC (0.33 [0.32–0.37] vs. 0.25 [0.24–0.33], p = 0.042). Both long-term groups had endothelial dysfunction compared with controls and atherosclerosis after 15 months. In conclusion, short-term hyperglycemia and dyslipidemia increase FVIII, independent of VWF. Long-term DM and HC increase VWF via endothelial dysfunction and atherosclerosis. Therefore, VWF seems to be a biomarker for advanced cardiovascular disease.

scholarly journals Homocysteine and Endothelial Dysfunction: A Link with Cardiovascular Disease

2000 ◽  
Vol 130 (2) ◽  
pp. 369S-372S ◽  
Author(s):  
Ian F. W. McDowell ◽  
Derek Lang
Keyword(s):  
Cardiovascular Disease ◽  
Endothelial Dysfunction

Abstract 166: Endothelial Overexpression of LOX-1 Increases Stroke Size in vivo

2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Alexander Akhmedov ◽  
Remo D Spescha ◽  
Francesco Paneni ◽  
Giovani G Camici ◽  
Thomas F Luescher
Keyword(s):  
Endothelial Cells ◽  
Ischemic Stroke ◽  
Endothelial Dysfunction ◽  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Cerebral Artery ◽  
Oxidized Ldl ◽  
Artery Occlusion ◽  
Cerebral Artery Occlusion ◽  
The Brain

Background— Stroke is one of the most common causes of death and long term disability worldwide primarily affecting the elderly population. Lectin-like oxidized LDL receptor 1 (LOX-1) is the receptor for oxidized LDL identified in endothelial cells. Binding of OxLDL to LOX-1 induces several cellular events in endothelial cells, such as activation of transcription factor NF-kB, upregulation of MCP-1, and reduction in intracellular NO. Accumulating evidence suggests that LOX-1 is involved in endothelial dysfunction, inflammation, atherogenesis, myocardial infarction, and intimal thickening after balloon catheter injury. Interestingly, a recent study demonstrated that acetylsalicylic acid (aspirin), which could prevent ischemic stroke, inhibited Ox-LDL-mediated LOX-1 expression in human coronary endothelial cells. The expression of LOX-1 was increased at a transient ischemic core site in the rat middle cerebral artery occlusion model. These data suggest that LOX-1 expression induces atherosclerosis in the brain and is the precipitating cause of ischemic stroke. Therefore, the goal of the present study was to investigate the role of endothelial LOX-1 in stroke using experimental mouse model. Methods and Results— 12-week-old male LOX-1TG generated recently in our group and wild-type (WT) mice were applied for a transient middle cerebral artery occlusion (MCAO) model to induce ischemia/reperfusion (I/R) brain injury. LOX-1TG mice developed 24h post-MCAO significantly larger infarcts in the brain compared to WT (81.51±8.84 vs. 46.41±10.13, n=7, p < 0.05) as assessed morphologically using Triphenyltetrazolium chloride (TTC) staining. Moreover, LOX-1TG showed higher neurological deficit in RotaRod (35.57±8.92 vs. 66.14±10.63, n=7, p < 0.05) and Bederson tests (2.22±0.14 vs. 1.25±0.30, n=9-12, p < 0.05) - two experimental physiological tests for neurological function. Conclusions— Thus, our data suggest that LOX-1 plays a critical role in the ischemic stroke when expressed at unphysiological levels. Such LOX-1 -associated phenotype could be due to the endothelial dysfunction. Therefore, LOX-1 may represent novel therapeutic targets for preventing ischemic stroke.

scholarly journals The Role of Endothelial Dysfunction in the Pathogenesis of Vascular Complications of Diabetes Mellitus - A High Priority Area of Investigation

2015 ◽  
Vol 22 (1) ◽  
pp. 61-66 ◽  
Author(s):  
Rodica Teodora Străchinariu
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Cardiovascular Disease ◽  
Endothelial Dysfunction ◽  
Vascular Complications ◽  
Noninvasive Methods ◽  
Cardiovascular Damage ◽  
Vasoactive Substances ◽  
Organ Systems ◽  
Increased Risk

Abstract Endothelium, the inner layer of the vasculature, represents the interface between blood and organ systems and it is active in the process of contraction and relaxation of vascular smooth muscle and in functions like secretion of vasoactive substances. Endothelial dysfunction is an important cause of cardiovascular disease. The function of the endothelium can be assessed by invasive and noninvasive methods. Endothelial cells produce vasoactive substances like endothelium derived relaxing factor, prostacyclin, nitric oxide, and endothelium derived hyperpolarizing factor. Diabetes mellitus is associated with an increased risk of cardiovascular diseases. Hyperglycemia leads to cardiovascular damage through different pathways, including the polyol and hexosamine pathways, generation of advanced glycation end products, and activation of protein kinase C. Together with hyperglycemia induced mitochondrial dysfunction and endoplasmic reticulum stress, all these can promote the accumulation of reactive oxygen species. The oxidative stress induced by hyperglycemia promotes endothelial dysfunction with an important role in micro and macro vascular disease. Insulin-resistance could be independently predictive of cardiovascular disease. Life style modification and pharmacotherapy could possibly ameliorate the effect of insulin resistance

scholarly journals Role of Endothelial Dysfunction in Cardiovascular Disease: A Review

2000 ◽  
Vol 5 (2) ◽  
pp. 59-66
Author(s):  
Amudha Kadirvelu ◽  
Chee Kok Han ◽  
Tan Kim Heung ◽  
Anna Maria Choy ◽  
Mustafa Mohd Rais ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Endothelial Dysfunction

scholarly journals Effect of Arterial Hypertension on the ICAM-1, VCAM-1 and Е-selectin Level in Type 2 Diabetes Patients

2021 ◽  
pp. 43-47
Author(s):  
Liliia Mogylnytska
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Cardiovascular Disease ◽  
Endothelial Dysfunction ◽  
Serum Level ◽  
Control Group ◽  
Regression Equations ◽  
Multifactor Regression ◽  
Diabetes Patients

Cardiovascular disease is the leading cause of death in diabetes mellitus. Endothelial dysfunction is the first step in the development of atherosclerotic vascular lesions, which underlies cardiovascular pathology, and adhesion molecules secreted by the endothelium during inflammatory changes are involved in the progression of this lesion. The objective: the serum level of adhesive molecules (ІCAM-1, VCAM-1, Е-selectin) in hypertensive and non-hypertensive type 2 diabetes patients as a marker of endothelial dysfunction and its relationship with other risk factors for cardiovascular disease was studied. Materials and methods. We examined 64 patients with type 2 diabetes, which were divided into two subgroups: the first subgroup – 41 hypertensive type 2 diabetes patients (age – 53,56±7,14 years, BMI – 32,2±87,4; HbA1c – 9,97±2,02%), the second subgroup – 23 nonhypertensive type 2 diabetes patients (age – 50,5±4,92 years, BMI – 25,4±5,22; HbA1c – 9,09±1,95%). The control group included 18 people without diabetes with normal blood pressure (age – 50,72±6,98 years, BMI – 24,71±4,88; HbA1c – 5,26±0,42%). The serum level was determined by immunoenzyme assay. The significance of the difference between the mean values was determined by the t-Student test. Multifactor regression analysis was used to assess the relationships between the studied factors. Results. We revealed an increase of serum levels of ІCAM-1, VCAM-1, Е-selectin in hypertensive (+71,62%, +68,42%, +66,95%, respectively) and non-hypertensive type 2 diabetes patients (+46,17%, +62,79%, +42,85%, respectively) compared with the control group (p<0,01). The serum concentration of ІCAM-1, Е-selectin was higher in hypertensive type 2 diabetes patients compared to non-hypertensive type 2 diabetes patients (+17,27%, +16,86%, respectively, p<0,01). There was a significant effect of Hb1Ac, lipids, insulin resistance on the serum level of ІCAM-1, VCAM-1, Е-selectin (p<0,01). The corresponding regression equations are derived. Conclusion. There is an increase of serum level of ІCAM-1, VCAM-1, Е-selectin in hypertensive and non-hypertensive type 2 diabetes patients, which indicates the development of endothelial dysfunction. Hypertension, hyperglycemia, dyslipidemia and insulin resistance contribute to the development of these changes.

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