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      Endothelial dysfunction: the early predictor of atherosclerosis

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          Abstract

          Abstract

          Since the discovery in the 1980s that nitric oxide (NO) is in fact the elusive endothelium-derived relaxing factor, it has become evident that NO is not only a major cardiovascular signalling molecule, but that changes in its bioavailability are crucial in determining whether atherosclerosis will develop or not. Sustained high levels of harmful circulating stimuli associated with cardiovascular risk factors such as diabetes mellitus elicit responses in endothelial cells that appear sequentially, namely endothelial cell activation and endothelial dysfunction (ED).

          ED, characterised by reduced NO bioavailability, is now recognised by many as an early, reversible precursor of atherosclerosis. The pathogenesis of ED is multifactorial; however, oxidative stress appears to be the common underlying cellular mechanism in the ensuing loss of vaso-active, inflammatory, haemostatic and redox homeostasis in the body’s vascular system. The role of ED as a pathophysiological link between early endothelial cell changes associated with cardiovascular risk factors and the development of ischaemic heart disease is of importance to basic scientists and clinicians alike.

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          Cardiovascular effects of secondhand smoke: nearly as large as smoking.

          Joaquin Barnoya, Stanton A. Glantz (2005)
          Secondhand smoke increases the risk of coronary heart disease by approximately 30%. This effect is larger than one would expect on the basis of the risks associated with active smoking and the relative doses of tobacco smoke delivered to smokers and nonsmokers. We conducted a literature review of the research describing the mechanistic effects of secondhand smoke on the cardiovascular system, emphasizing research published since 1995, and compared the effects of secondhand smoke with the effects of active smoking. Evidence is rapidly accumulating that the cardiovascular system--platelet and endothelial function, arterial stiffness, atherosclerosis, oxidative stress, inflammation, heart rate variability, energy metabolism, and increased infarct size--is exquisitely sensitive to the toxins in secondhand smoke. The effects of even brief (minutes to hours) passive smoking are often nearly as large (averaging 80% to 90%) as chronic active smoking. The effects of secondhand smoke are substantial and rapid, explaining the relatively large risks that have been reported in epidemiological studies.
          Article 0 comments Cited 211 times – based on 0 reviews     Review now
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            Role of TNF-α in vascular dysfunction

            Hanrui Zhang, Yoonjung Park, Junxi Wu … (2009)
            Healthy vascular function is primarily regulated by several factors including EDRF (endothelium-dependent relaxing factor), EDCF (endothelium-dependent contracting factor) and EDHF (endothelium-dependent hyperpolarizing factor). Vascular dysfunction or injury induced by aging, smoking, inflammation, trauma, hyperlipidaemia and hyperglycaemia are among a myriad of risk factors that may contribute to the pathogenesis of many cardiovascular diseases, such as hypertension, diabetes and atherosclerosis. However, the exact mechanisms underlying the impaired vascular activity remain unresolved and there is no current scientific consensus. Accumulating evidence suggests that the inflammatory cytokine TNF (tumour necrosis factor)-α plays a pivotal role in the disruption of macrovascular and microvascular circulation both in vivo and in vitro. AGEs (advanced glycation end-products)/RAGE (receptor for AGEs), LOX-1 [lectin-like oxidized low-density lipoprotein receptor-1) and NF-κB (nuclear factor κB) signalling play key roles in TNF-α expression through an increase in circulating and/or local vascular TNF-α production. The increase in TNF-α expression induces the production of ROS (reactive oxygen species), resulting in endothelial dysfunction in many pathophysiological conditions. Lipid metabolism, dietary supplements and physical activity affect TNF-α expression. The interaction between TNF-α and stem cells is also important in terms of vascular repair or regeneration. Careful scrutiny of these factors may help elucidate the mechanisms that induce vascular dysfunction. The focus of the present review is to summarize recent evidence showing the role of TNF-α in vascular dysfunction in cardiovascular disease. We believe these findings may prompt new directions for targeting inflammation in future therapies.
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              Mechanisms of Increased Vascular Superoxide Production in Human Diabetes Mellitus: Role of NAD(P)H Oxidase and Endothelial Nitric Oxide Synthase

              Tomasz J. Guzik, Shafi Mussa, Daniela Gastaldi … (2002)
              Background — Increased superoxide production contributes to reduced vascular nitric oxide (NO) bioactivity and endothelial dysfunction in experimental models of diabetes. We characterized the sources and mechanisms underlying vascular superoxide production in human blood vessels from diabetic patients with coronary artery disease compared with nondiabetic patients. Methods and Results — Vascular superoxide production was quantified in both saphenous veins and internal mammary arteries from 45 diabetic and 45 matched nondiabetic patients undergoing coronary artery bypass surgery. NAD(P)H-dependent oxidases were important sources of vascular superoxide in both diabetic and nondiabetic patients, but both the activity of this enzyme system and the levels of NAD(P)H oxidase protein subunits (p22phox, p67phox, and p47phox) were significantly increased in diabetic veins and arteries. In nondiabetic vessels, endothelial NO synthase produced NO that scavenged superoxide. However, in diabetic vessels, the endothelium was an additional net source of superoxide production because of dysfunctional endothelial NO synthase that was corrected by intracellular tetrahydrobiopterin supplementation. Furthermore, increased superoxide production in diabetes was abrogated by the protein kinase C inhibitor chelerythrine. Conclusions — These observations suggest important roles for NAD(P)H oxidases, endothelial NO synthase uncoupling, and protein kinase C signaling in mediating increased vascular superoxide production and endothelial dysfunction in human diabetes mellitus.
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                Author and article information

                Contributors
                Mashudu Mudau
                Amanda Genis
                Amanda Lochner
                Hans Strijdom
                Journal
                Journal ID (nlm-ta): Cardiovasc J Afr
                Journal ID (iso-abbrev): Cardiovasc J Afr
                Journal ID (publisher-id): TBC
                Title: Cardiovascular Journal of Africa
                Publisher: Clinics Cardive Publishing
                ISSN (Print): 1995-1892
                ISSN (Electronic): 1680-0745
                Publication date (Print): May 2012
                Volume: 23
                Issue: 4
                Pages: 222-231
                Affiliations
                Department of Biomedical Sciences, Division of Medical Physiology, Faculty of Health Sciences, Stellenbosch University, Stellenbosch, South Africa
                Department of Biomedical Sciences, Division of Medical Physiology, Faculty of Health Sciences, Stellenbosch University, Stellenbosch, South Africa
                Department of Biomedical Sciences, Division of Medical Physiology, Faculty of Health Sciences, Stellenbosch University, Stellenbosch, South Africa
                Department of Biomedical Sciences, Division of Medical Physiology, Faculty of Health Sciences, Stellenbosch University, Stellenbosch, South Africa
                Article
                DOI: 10.5830/CVJA-2011-068
                PMC ID: 3721957
                PubMed ID: 22614668
                SO-VID: 1d2c368e-eded-400f-af63-d30549da849c
                Copyright © Copyright © 2010 Clinics Cardive Publishing
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 7 June 2011
                Date accepted : 11 November 2011
                Categories
                Subject: Review Article

                Keywords: endothelium,endothelial dysfunction,nitric oxide bioavailability,enos uncoupling,oxidative stress,atherosclerosis
                Data availability:
                Keywords: endothelium, endothelial dysfunction, nitric oxide bioavailability, enos uncoupling, oxidative stress, atherosclerosis

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