The Effects of Angiotensin II Infusion on the Mechanical Response and Microstructural Organization of Mouse Aorta

2010 ◽  
Author(s):  
Darren Haskett ◽  
Marie Fouts ◽  
Urs Utzinger ◽  
Doug Larson ◽  
Mohamad Azhar ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Vascular Disease ◽  
Mechanical Response ◽  
Vascular Inflammation ◽  
Vascular Diseases ◽  
The United States ◽  
Matrix Remodeling ◽  
Atherosclerotic Vascular Disease ◽  
Thoracic And Abdominal ◽  
Aortic Remodeling

Vascular diseases such as aneurysm and aortic dissection account for almost 16,000 deaths in the United States annually. In both of these diseases vascular inflammation is a common pathogenic factor. Another common pathologic feature of vascular disease includes structural matrix remodeling. It is also increasingly believed that inflammation may play a key role in the formation and progression of atherosclerotic vascular disease. Angiotensin II (AngII), a potent vasopressor, is also a strong inducer of vascular inflammation and aortic remodeling in atherosclerosis-prone mice. Based on this knowledge studies have been conducted using subcutaneous AngII infusion in order to produce aortic remodeling and aneurysm formation, with acute thoracic and abdominal aortic dissections [1].

scholarly journals Anti-Inflammatory Effects of Interleukin-19 in Vascular Disease

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Ross N. England ◽  
Michael V. Autieri
Keyword(s):  
Vascular Disease ◽  
Vascular Inflammation ◽  
Vascular Diseases ◽  
Lipid Lowering ◽  
Western World ◽  
Atherosclerotic Vascular Disease ◽  
Therapeutic Modalities ◽  
Number Of Patients ◽  
Rational Therapy ◽  
Health And Disease

Despite aggressive dietary modification, lipid-lowering medications, and other interventional medical therapy, vascular disease continues to be a leading cause of mortality in the western world. It is a significant medical and socioeconomic problem contributing to mortality of multiple diseases including myocardial infarction, stroke, renal failure, and peripheral vascular disease. Morbidity and mortality of vascular disease are expected to worsen with the increasing number of patients with comorbid conditions such as obesity, metabolic syndrome, and diabetes mellitus type 2. Vascular diseases such as atherosclerosis, restenosis, and allograft vasculopathy are recognized to be driven by inflammation, and as such, cytokines which mediate inflammation not only represent important targets of rational therapy, but also can be considered as possible therapeutic modalities themselves. In this paper, we will examine the role of inflammatory cytokines and lymphocyteTh1/Th2 polarity in vascular inflammation, with a focus on atherosclerotic vascular disease. We will then introduce a recently describedTh2 interleukin, interleukin-19 (IL-19), as a previously unrecognized mediator of vascular inflammatory disorders. We will review our current understanding of this interleukin in health and disease and present the possibility that IL-19 could represent a potential therapeutic to combat vascular inflammatory disease.

Endothelial Dysfunction and Inflammatory Markers of Vascular Disease

2020 ◽  
Vol 19 (3) ◽  
pp. 243-249 ◽  
Author(s):  
Sevket Balta
Keyword(s):  
Endothelial Dysfunction ◽  
Vascular Disease ◽  
Inflammatory Markers ◽  
Vascular Diseases ◽  
Intima Media Thickness ◽  
Carotid Intima Media Thickness ◽  
Non Invasive ◽  
Von Willebrand ◽  
The Relationship ◽  
Willebrand Factor

: Vascular diseases are the main reason for morbidity and mortality worldwide. As we know, the earlier phase of vascular diseases is endothelial dysfunction in humans, the endothelial tissues play an important role in inflammation, coagulation, and angiogenesis, via organizing ligand-receptor associations and the various mediators’ secretion. We can use many inflammatory non-invasive tests (flowmediated dilatation, epicedial fat thickness, carotid-intima media thickness, arterial stiffness and anklebrachial index) for assessing the endothelial function. In addition, many biomarkers (ischemia modified albumin, pentraxin-3, E-selectin, angiopoietin, endothelial cell specific molecule 1, asymmetrical dimethylarginine, von Willebrand factor, endothelial microparticles and endothelial progenitor cells) can be used to evaluate endothelial dysfunction. We have focused on the relationship between endothelial dysfunction and inflammatory markers of vascular disease in this review.

Oxidized ApoC1 on MALDI-TOF and glycated-ApoA1 band on gradient gel as potential diagnostic tools for atherosclerotic vascular disease

2013 ◽  
Vol 420 ◽  
pp. 69-75 ◽  
Author(s):  
Chiz-Tzung Chang ◽  
Hsin-Yi Liao ◽  
Chia-Ming Chang ◽  
Chia-Ying Chen ◽  
Chu-Huang Chen ◽  
...  
Keyword(s):  
Vascular Disease ◽  
Diagnostic Tools ◽  
Atherosclerotic Vascular Disease ◽  
Maldi Tof

scholarly journals The Epigenome in Atherosclerosis

2020 ◽  
Author(s):  
Sarah Costantino ◽  
Francesco Paneni
Keyword(s):  
Vascular Disease ◽  
Posttranslational Modifications ◽  
Epigenetic Modifications ◽  
Atherosclerotic Vascular Disease ◽  
Biological Regulation ◽  
Genetic Changes ◽  
Epigenetic Biomarkers ◽  
The Individual ◽  
Novel Therapeutic Strategies ◽  
Vascular Oxidative Stress

AbstractEmerging evidence suggests the growing importance of “nongenetic factors” in the pathogenesis of atherosclerotic vascular disease. Indeed, the inherited genome determines only part of the risk profile as genomic approaches do not take into account additional layers of biological regulation by “epi”-genetic changes. Epigenetic modifications are defined as plastic chemical changes of DNA/histone complexes which critically affect gene activity without altering the DNA sequence. These modifications include DNA methylation, histone posttranslational modifications, and non-coding RNAs and have the ability to modulate gene expression at both transcriptional and posttranscriptional level. Notably, epigenetic signals are mainly induced by environmental factors (i.e., pollution, smoking, noise) and, once acquired, may be transmitted to the offspring. The inheritance of adverse epigenetic changes may lead to premature deregulation of pathways involved in vascular damage and endothelial dysfunction. Here, we describe the emerging role of epigenetic modifications as fine-tuners of gene transcription in atherosclerosis. Specifically, the following aspects are described in detail: (1) discovery and impact of the epigenome in cardiovascular disease, (2) the epigenetic landscape in atherosclerosis; (3) inheritance of epigenetic signals and premature vascular disease; (4) epigenetic control of lipid metabolism, vascular oxidative stress, inflammation, autophagy, and apoptosis; (5) epigenetic biomarkers in patients with atherosclerosis; (6) novel therapeutic strategies to modulate epigenetic marks. Understanding the individual epigenetic profile may pave the way for new approaches to determine cardiovascular risk and to develop personalized therapies to treat atherosclerosis and its complications.

Abstract TP297: Predictors of Intracranial Hemorrhage in Patients with Atherosclerotic Vascular Disease: Observations from the TRA 2°P-TIMI 50 Trial

Stroke ◽  
2013 ◽  
Vol 44 (suppl_1) ◽  
Author(s):  
Marc P Bonaca ◽  
Jay P Mohr ◽  
Mark J Alberts ◽  
Sebastian F Ameriso ◽  
Graeme J Hankey ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Vascular Disease ◽  
Renal Dysfunction ◽  
Intracranial Hemorrhage ◽  
Rare Event ◽  
Arterial Disease ◽  
Male Gender ◽  
Atherosclerotic Vascular Disease ◽  
Clinical Predictors ◽  
History Of

Intracranial hemorrhage (ICH) is a rare event that is difficult to predict and often has devastating consequences. Clinical predictors of ICH in stable patients with atherosclerosis are not well described. Methods: We evaluated the clinical correlates of ICH risk in patients randomized to placebo (N=13,166) in the TRA 2°P-TIMI 50 trial, a multinational trial of patients with atherothrombosis randomized to vorapaxar or placebo added to standard therapy. Eligible patients had a history of myocardial infarction, peripheral arterial disease, or recent ischemic stroke (2 wks to 12 mo.). ICH was adjudicated by an independent CEC. Results: A total of 53 ICH events (0.5% at 3 years) occurred during follow up in the placebo group. 94% of patients were receiving aspirin, 5% a thienopyridine alone, and 57% dual antiplatelet therapy. Overall, age, sex, prior ischemic stroke, and renal dysfunction were significantly associated with ICH (Table 1). After adjustment age, male gender, and prior ischemic stroke remained significantly associated with an increased hazard of ICH (Figure 1). Notably, the predictors differed between qualifying groups. After adjustment renal dysfunction (p=0.018) and diabetes (p=0.073) were associated with ICH in the MI/PAD group. In contrast, only male gender was associated with ICH in the CVD group (p=0.048). Conclusions: Advanced age, male gender, and history of ischemic stroke are associated with an increased hazard of ICH in patients with a history of atherothrombosis. Predictors of ICH vary depending on background vascular disease. In patients with MI/PAD and no recent stroke, traditional risk factors including diabetes and renal dysfunction are associated with ICH.

scholarly journals Angiotensin II, Hypercholesterolemia, and Vascular Smooth Muscle Cells: A Perfect Trio for Vascular Pathology

2020 ◽  
Vol 21 (12) ◽  
pp. 4525
Author(s):  
Amanda St. Paul ◽  
Cali B. Corbett ◽  
Rachael Okune ◽  
Michael V. Autieri
Keyword(s):  
Blood Pressure ◽  
Cardiovascular Disease ◽  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Vascular Smooth Muscle ◽  
Vascular Diseases ◽  
Reduce Blood Pressure ◽  
Vascular Pathology ◽  
Lipid Lowering ◽  
Ang Ii

Cardiovascular disease is the leading cause of morbidity and mortality in the Western and developing world, and the incidence of cardiovascular disease is increasing with the longer lifespan afforded by our modern lifestyle. Vascular diseases including coronary heart disease, high blood pressure, and stroke comprise the majority of cardiovascular diseases, and therefore represent a significant medical and socioeconomic burden on our society. It may not be surprising that these conditions overlap and potentiate each other when we consider the many cellular and molecular similarities between them. These intersecting points are manifested in clinical studies in which lipid lowering therapies reduce blood pressure, and anti-hypertensive medications reduce atherosclerotic plaque. At the molecular level, the vascular smooth muscle cell (VSMC) is the target, integrator, and effector cell of both atherogenic and the major effector protein of the hypertensive signal Angiotensin II (Ang II). Together, these signals can potentiate each other and prime the artery and exacerbate hypertension and atherosclerosis. Therefore, VSMCs are the fulcrum in progression of these diseases and, therefore, understanding the effects of atherogenic stimuli and Ang II on the VSMC is key to understanding and treating atherosclerosis and hypertension. In this review, we will examine studies in which hypertension and atherosclerosis intersect on the VSMC, and illustrate common pathways between these two diseases and vascular aging.

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