Nitric oxide and the resolution of inflammation: implications for atherosclerosis

Shaw, Catherine; Taylor, Emma; Megson, Ian L.; Rossi, Adriano G.

doi:10.1590/s0074-02762005000900012

Cited by 21 publications

(12 citation statements)

References 50 publications

(49 reference statements)

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“…Recent studies have indicated that NO modulates apoptosis, or programmed cell death, in several cell types, including inflammatory cells (Shaw et al 2005). Apoptosis, characterized by a series of morphological and biochemical alterations, eliminates excess or unwanted cells from tissue without inducing an inflammatory reaction to maintain tissue homeostasis (Vignali et al 2002).…”

Section: Molecular Mechanisms Of Apoptotic Cell Death Induced By Nomentioning

confidence: 99%

Role of iron overload-induced macrophage apoptosis in the pathogenesis of peritoneal endometriosis

Pirdel¹,

Pirdel²

2014

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This article presents an overview of the involvement of iron overload-induced nitric oxide (NO) overproduction in apoptosis of peritoneal macrophages of women with endometriosis. We have postulated that the peritoneal iron overload originated from retrograde menstruation or bleeding lesions in the ectopic endometrium, which may contribute to the development of endometriosis by a wide range of mechanisms, including oxidative damage and chronic inflammation. Excessive NO production may also be associated with impaired clearance of endometrial cells by macrophages, which promotes cell growth in the peritoneal cavity. Therefore, further research of the mechanisms and consequences of macrophage apoptosis in endometriosis helps discover novel therapeutic strategies that are designed to prevent progression of endometriosis.

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Section: Molecular Mechanisms Of Apoptotic Cell Death Induced By Nomentioning

confidence: 99%

Role of iron overload-induced macrophage apoptosis in the pathogenesis of peritoneal endometriosis

Pirdel¹,

Pirdel²

2014

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“…This process is particularly important in the vascular system, where they can damage the endothelium by peroxidation and initiate the atherosclerotic lesion. 23 NO is known as a vascular smooth muscle tone controller, it inhibits platelet activation, modulates apoptosis and inflammatory cell aggregation and activation at low concentrations. On the other hand, NO can react with superoxide anion (O 2 ) to form peroxynitrite (ONOO -), which is highly cytotoxic.…”

Section: Lipid Peroxidation and Mdamentioning

confidence: 99%

“…Associated with other factors, the overproduction of NO is one of the most important issues involved in the development of lipid atherosclerotic plaques. 23 In the last 20 years, MDA has been recognized as an important lipid peroxidation indicator, since subjects affected by several diseases have the MDA levels increased. [3][4][5]24 The involvement of lipid peroxidation in cancer is a good example; cancer results from the accumulation of the multiple mutations in key growth regulatory genes.…”

Section: Lipid Peroxidation and Mdamentioning

confidence: 99%

Importance of the lipid peroxidation biomarkers and methodological aspects FOR malondialdehyde quantification

Grotto¹,

Maria²,

Valentini³

et al. 2009

Quím. Nova

322

237

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Recebido em 16/2/07; aceito em 7/3/08; publicado na web em 31/10/08Free radicals induce lipid peroxidation, playing an important role in patho logical processes. The injury mediated by free radicals can be measured by conjugated dienes, malon dial dehyde, 4-hydroxynonenal, and others. However, malondialdehyde has been pointed out as the main product to evaluate lipid peroxidation. Most assays determine malondialdehyde by its reaction with thiobarbituric acid, which can be mea sured by indirect (spectrometry) and direct methodologies (chromatography). Though there is some controversy among the methodologies, the selective HPLC-based assays provide a more reliable lipid peroxidation measure. This review describes significant aspects about MDA deter mination, its importance in pathologies and biological samples treatment.

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“…Because of its proapoptotic properties, NO has the potential to promote the resolution of inflammation during the atherosclerotic process and might, therefore, be a promising target for therapeutic manipulation. 24,25 Hypercholesterolemic rabbits treated with the NOS substrate, L-arginine, have elevated numbers of apoptotic cells, particularly macrophages, in the intimal lesions. 26 Furthermore, regression of atheroma was also observed in this model, reinforcing its potential as a therapeutic target.…”

Section: No Signaling In the Resolution Of Inflammationmentioning

confidence: 99%

Mechanisms of Resolution of Inflammation

Maskrey

Megson

Whitfield

et al. 2011

ATVB

147

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Abstract-The inflammatory response is an integral part of the innate immune mechanism that is triggered in response to a real or perceived threat to tissue homeostasis, with a primary aim of neutralizing infectious agents and initiating repair to damaged tissue. By design, inflammation is a finite process that resolves as soon as the threat of infection abates and sufficient repair to the tissue is complete. Resolution of inflammation involves apoptosis and subsequent clearance of activated inflammatory cells -a tightly regulated event. Chronic inflammation is a characteristic feature in virtually all inflammatory diseases, including atherosclerosis, and it is becoming increasingly clear that derangement of the processes usually involved in resolution of inflammation is an underlying feature of chronic inflammatory conditions. This review will draw on evidence from a range of diseases in which dysregulated inflammation is important, with particular emphasis on cardiovascular disease. (Arterioscler Thromb Vasc Biol. 2011;31:1001-1006.)Key Words: atherosclerosis Ⅲ eicosanoids Ⅲ lipids Ⅲ NO Ⅲ resolution of inflammation I nflammation is a primary component of the immune system that is triggered by any stimulus that poses a real or perceived threat to tissue homeostasis. 1 The acute inflammatory process is characterized by rapid recruitment of granulocytes (ie, neutrophils, eosinophils, and basophils) to the inflammatory site; the relative contribution of these cell types is dependent on the location of the inflammatory site in question. The migration of granulocytes to inflammatory loci is a necessary requirement for the neutralization and removal of deleterious agents; these cells play a key role in the defense against bacterial, fungal, and viral infections and in resistance to parasitic invasion and the allergic response. Resolution of inflammation is perceived to occur by elimination of granulocytes and the eventual return of tissue mononuclear cell (macrophage and lymphocyte) numbers to basal levels. 2 For effective resolution to occur, cessation of proinflammatory signaling is a prerequisite that pre-empts removal of infiltrating granulocytes. During spontaneous resolution, neutrophils undergo apoptosis, a highly regulated cell death mechanism that prevents the release of histotoxic cellular contents. 3 Alterations in neutrophil cell surface markers and morphological changes during apoptosis correlate with increased recognition by professional phagocytes, such as macrophages, that mediate effective clearance of dying cells. 3,4 It is accepted that the resolution process is active, rather than passive, and is controlled by a range of tightly regulated biochemical and cellular mechanisms. 2 The acute inflammatory response is self-limiting and normally results in tissue restoration and the return of tissue homeostasis. Persistent inflammatory stimuli or dysregulation of mechanisms of the resolution phase results in chronic inflammation, 2 recognized to be a key underlying factor in the progression of a range of d...

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Nitric oxide and the resolution of inflammation: implications for atherosclerosis

Abstract: The ubiquitous free radical, nitric oxide (NO)

Cited by 21 publications

References 50 publications

Role of iron overload-induced macrophage apoptosis in the pathogenesis of peritoneal endometriosis

Role of iron overload-induced macrophage apoptosis in the pathogenesis of peritoneal endometriosis

Importance of the lipid peroxidation biomarkers and methodological aspects FOR malondialdehyde quantification

Mechanisms of Resolution of Inflammation

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