Soluble integrin adhesion receptors and atherosclerosis: much heat and a little light?

Hillis, Graham S.

doi:10.1038/sj.jhh.1001569

Cited by 9 publications

(5 citation statements)

References 56 publications

(76 reference statements)

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“…The finding that soluble forms of adhesion molecules are found in circulation has led to considerable interest as being potential markers for atherosclerosis and cardiovascular risk [66]. Leucocyte dyapedesis is then regulated by chemotactic molecules.…”

Section: Atherosclerosis As An Inflammatory Diseasementioning

confidence: 99%

Macroangiopathy in Adults and Children with Diabetes: From Molecular Mechanisms to Vascular Damage (Part 1)

Marzio¹,

Mohn²,

Mokini³

et al. 2006

Horm Metab Res

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Type 2 diabetes mellitus (T2DM) is an increasing problem in childhood; however type 1 diabetes mellitus (T1DM) remains by far the most common type of diabetes in this age group. In this review we will focus on T1DM, because this will have the greatest implication for patients diagnosed in childhood. During the atherosclerotic process, several molecular, receptorial and cellular factors provide a continous mechanism of vascular damage. In diabetic children this state seems to be enhanced and facilitated so that accelerated atherosclerosis is associated with an increased risk of cardiovascular events in respect to the non diabetic population. Hyperglycemia PER SE and associated with diabetes is an important risk factor for atherosclerosis. At present a substantial part of children with diabetes do not reach satisfactory glycemic control. Other risk factors for the development and progression of atherosclerosis may be inherited or develop in the course of the disease: hypertension, dyslipidemia, insulin resistance, obesity, cigarette smoking, physical inactivity, disturbance of platelet function, coagulation and fibrinolysis. The development and progression of atherosclerosis should be blocked at an early age, if possible. Primary prevention to all risk factors for cardiovascular disease is important and intervention is indicated if necessary. At the moment the best therapeutic strategy is to maintain metabolic control at a physiologic level and perform screening and early intervention for vascular complications.

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Section: Atherosclerosis As An Inflammatory Diseasementioning

confidence: 99%

Macroangiopathy in Adults and Children with Diabetes: From Molecular Mechanisms to Vascular Damage (Part 1)

Marzio¹,

Mohn²,

Mokini³

et al. 2006

Horm Metab Res

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show abstract

“…Atherosclerosis is considered a chronic inflammatory disease involving a complex interplay between vascular cells and infiltrating immune cells (e.g., macrophages) initiated by endothelial dysfunction followed by inflammatory cell infiltration and lipid accumulation (16,29,30). Macrophages infiltrating into endothelial and smooth muscle cells secrete several proinflammatory cytokines, such as TNF-␣, IL-6, and interferon (IFN)-␥, which can exacerbate the risk of atherosclerotic vascular diseases (22,30).…”

mentioning

confidence: 99%

Adiponectin abates diabetes-induced endothelial dysfunction by suppressing oxidative stress, adhesion molecules, and inflammation in type 2 diabetic mice

Lee

Zhang

Chen

et al. 2012

American Journal of Physiology-Heart and Circulatory Physiology

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; db/db) mice and studied vascular function of the aorta ex vivo. Ad-APN improved endothelial-dependent vasodilation in db/db mice compared with Ad␤gal, whereas Ad-APN had no further improvement on endothelial function in control mice. This improvement was completely inhibited by a nitric oxide synthase inhibitor (N G -nitro-L-arginine methyl ester). Serum triglyceride and total cholesterol levels were increased in db/db mice, and Ad-APN significantly reduced triglyceride levels but not total cholesterol levels. Immunoblot results showed that interferon-␥, gp91 phox , and nitrotyrosine were markedly increased in the aorta of db/db mice. Ad-APN treatment decreased the expression of these proteins. In addition, mRNA expression of TNF-␣, IL-6, and ICAM-1 was elevated in db/db mice, and Ad-APN treatment decreased these expressions in the aorta. Our findings suggest that APN may contribute to an increase in nitric oxide bioavailability by decreasing superoxide production as well as by inhibiting inflammation and adhesion molecules in the aorta in type 2 diabetic mice. cardiovascular disease; adipokine; superoxide; vascular biology; adenovirus

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“…It should be stressed at this moment that the age-dependent decrease in P-selectin should be considered as the beneficial process for healthy people, as this molecule mediates various elements of proinflammatory cascade and contributes to vascular disorders [43]. The lack of the correlation regarding P-selectin in varicose patients, in combination with positive relationships for ICAM-1, VCAM-1, and ET-1 (all are actively involved in atherosclerosis [44, 45]), implies that varicosity makes a serum more proinflammatory, and thus it may be partly responsible for the development of certain age-related pathologies.…”

Section: Discussionmentioning

confidence: 99%

Serum from Varicose Patients Induces Senescence‐Related Dysfunction of Vascular Endothelium Generating Local and Systemic Proinflammatory Conditions

Mikuła-Pietrasik

Uruski

Aniukiewicz

et al. 2016

Oxidative Medicine and Cellular Longevity

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Although the role of endothelium in varicose vein development is indisputable, the effect of the pathology on biological properties of endothelial cells remains unclear. Here we examined if the presence of varicose veins affects senescence of endothelial cells (HUVECs) and, if so, what will be the local and systemic outcome of this effect. Experiments showed that HUVECs subjected to serum from varicose patients display improved proliferation, increased expression of senescence marker, SA-β-Gal, and increased generation of reactive oxygen species (ROS), as compared with serum from healthy donors. Both increased SA-β-Gal activity and ROS release were mediated by TGF-β1, the concentration of which in varicose serum was elevated and the activity of which in vitro was prevented using specific neutralizing antibody. Senescent HUVECs exposed to varicose serum generated increased amounts of ICAM-1, VCAM-1, P-selectin, uPA, PAI-1, and ET-1. Direct comparison of sera from varicose and healthy donors showed that pathological serum contained increased level of ICAM-1, VCAM-1, P-selectin, uPA, and ET-1. Calendar age of healthy subjects correlated positively with serum uPA and negatively with P-selectin. Age of varicose patients correlated positively with ICAM-1, VCAM-1, and ET-1. Collectively, our findings indicate that the presence of varicose veins causes a senescence-related dysfunction of vascular endothelium, which leads to the development of local and systemic proinflammatory environment.

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Soluble integrin adhesion receptors and atherosclerosis: much heat and a little light?

Cited by 9 publications

References 56 publications

Macroangiopathy in Adults and Children with Diabetes: From Molecular Mechanisms to Vascular Damage (Part 1)

Macroangiopathy in Adults and Children with Diabetes: From Molecular Mechanisms to Vascular Damage (Part 1)

Adiponectin abates diabetes-induced endothelial dysfunction by suppressing oxidative stress, adhesion molecules, and inflammation in type 2 diabetic mice

Serum from Varicose Patients Induces Senescence‐Related Dysfunction of Vascular Endothelium Generating Local and Systemic Proinflammatory Conditions

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