Physiology and pathophysiology of oxLDL uptake by vascular wall cells in atherosclerosis

Pietro, Natalia Di; Formoso, Gloria; Pandolfi, Assunta

doi:10.1016/j.vph.2016.05.013

Cited by 213 publications

(146 citation statements)

References 116 publications

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“…Ox-LDL uptake and monocyte-endothelial cells adhesion play important roles in promoting atherosclerosis (Mestas and Ley, 2008; Di Pietro et al, 2016). Binding and endocytosis of ox-LDL is considered the primary function of LOX-1 in endothelial cells (Sawamura et al, 1997) and macrophages (Li et al, 2009).…”

Section: Discussionmentioning

confidence: 99%

Dihydrotanshinone I Attenuates Atherosclerosis in ApoE-Deficient Mice: Role of NOX4/NF-κB Mediated Lectin-Like Oxidized LDL Receptor-1 (LOX-1) of the Endothelium

Zhao

Gao

et al. 2016

Front. Pharmacol.

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Dihydrotanshinone I (DHT) is a natural compound extracted from Salvia miltiorrhiza Bunge which has been widely used for treating cardiovascular diseases. However, its role in atherosclerosis remains unclear. In this study, the effect of DHT on atherosclerosis were investigated using apolipoprotein E-deficient (ApoE-/-) mice and endothelial cells. In lipopolysaccharide (LPS)-stimulated human umbilical vein endothelial cells (HUVECs), DHT (10 nM) decreased lectin-like ox-LDL receptor-1 (LOX-1) and NADPH oxidase 4 (NOX4) expression, reactive oxygen species (ROS) production, NF-κB nuclear translocation, ox-LDL endocytosis and monocytes adhesion. Silence NOX4 inhibited LPS-induced LOX-1 expression, NF-κB nuclear translocation, ox-LDL endocytosis and monocytes adhesion. In ApoE-/- mice fed with an atherogenic diet, DHT (10 and 25 mg kg-1) significantly attenuated atherosclerotic plaque formation, altered serum lipid profile, decreased oxidative stress and shrunk necrotic core areas. The enhanced expression of LOX-1, NOX4, and NF-κB in aorta was also dramatically inhibited by DHT. In conclusion, these results suggested that DHT showed anti-atherosclerotic activity through inhibition of LOX-1 mediated by NOX4/NF-κB signaling pathways both in vitro and in vivo. This finding suggested that DHT might be used as a potential vascular protective candidate for the treatment of atherosclerosis.

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Section: Discussionmentioning

confidence: 99%

Dihydrotanshinone I Attenuates Atherosclerosis in ApoE-Deficient Mice: Role of NOX4/NF-κB Mediated Lectin-Like Oxidized LDL Receptor-1 (LOX-1) of the Endothelium

Zhao

Gao

et al. 2016

Front. Pharmacol.

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“…In atherogenesis, macrophage activation and class switching are critical for foam cell formation (139). Recent data suggest that this activity is associated with CD36 activation, which works as a scavenging receptor and is a critical molecule in internalization of oxo-LDL (140).…”

Section: Pro-resolving Mediators Periodontitis and Systemic Diseasementioning

confidence: 99%

Pro-resolving mediators in the regulation of periodontal disease

Dyke¹

2017

Molecular Aspects of Medicine

126

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Periodontitis is an inflammatory disease of the supporting structures of the dentition that is initiated by bacterial that form a biofilm on the surface of the teeth. The pathogenesis of the disease is a result of complex interactions between the biofilm and the host response that results in dysbiosis of the microbiome and dysregulation of the inflammatory response. Current data suggest that the excess inflammation associated with periodontitis is due to a failure of resolution of inflammation pathways. In this review, the relationship between inflammation and microbial dysbiosis is examined in the context of pro-inflammation and pro-resolution mediators and their ability to modify the course of disease. The impact of local oral inflammation on systemic inflammation and the relationship of periodontitis to other inflammatory diseases, including type 2 diabetes and cardiovascular disease is reviewed. Active resolvers of inflammation, including the lipoxins and resolvins, show great promise as therapeutics for the treatment of periodontitis and other inflammatory diseases.

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“…Some of these are intensely atherogenic such as malonyldialdehyde, the final products of advanced glycation or the protein products of advanced oxidation; they trigger the atherosclerotic process and damage the intimal wall of the arteries, causing a vascular inflammatory response and expression of leucocyte adhesion molecules, followed by migration of inflammatory cells into the sub-endothelial space. Oxidized LDL, in its turn, stimulates the formation of foamy cells and releases into circulation a great number of pro-inflammatory cytokines, which may destabilize plaque and increase the risk of ischemic cardiomyopathy (46,47).…”

Section: Diminished Erythrocyte Activity In the Intracellular Antioximentioning

confidence: 99%

Erythrocyte Alterations and Increased Cardiovascular Risk in Chronic Renal Failure

et al. 2017

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Patients suffering from chronic renal failure have a higher burden of cardiovascular events, which increases in a dose-dependent fashion as renal function worsens. Increased cardiovascular risk in these patients is thought to be mediated by the simultaneous presence of both traditional and non-traditional cardiovascular risk factors, the latter being associated with renal impairment. Red blood cells are usually considered as carries of nutrients for tissues and respiratory gases, less so as compartments essential to vascular integrity. However, erythrocyte number, size, and integrity seem to severely affect cardiovascular morbidity and mortality as established in recent clinical studies with large patient cohorts. In particular, the role of red blood cells in chronic renal failure tends only to be considered exclusively in relation to a change in their number. However, these cells in the uremic milieu are prone to many alterations, which may adversely affect the cardiovascular system. In this review, we highlight the main qualitative erythrocyte alterations that may have a pathophysiologic role in the elevated cardiovascular risk of chronic renal failure.

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Physiology and pathophysiology of oxLDL uptake by vascular wall cells in atherosclerosis

Cited by 213 publications

References 116 publications

Dihydrotanshinone I Attenuates Atherosclerosis in ApoE-Deficient Mice: Role of NOX4/NF-κB Mediated Lectin-Like Oxidized LDL Receptor-1 (LOX-1) of the Endothelium

Dihydrotanshinone I Attenuates Atherosclerosis in ApoE-Deficient Mice: Role of NOX4/NF-κB Mediated Lectin-Like Oxidized LDL Receptor-1 (LOX-1) of the Endothelium

Pro-resolving mediators in the regulation of periodontal disease

Erythrocyte Alterations and Increased Cardiovascular Risk in Chronic Renal Failure

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