Investigation of Sudan IV staining areas in aortas of infants and children: Possible prelesional stages of atherogenesis

Torzewski, Michael; Navarro, Bianca; Cheng, Fei; Canisius, Antje; Schmidt, Talkea; Bhakdi, Sucharit; Urban, R.; Lackner, Karl J.

doi:10.1016/j.atherosclerosis.2009.01.038

Cited by 12 publications

(21 citation statements)

References 35 publications

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“…monocytes and macrophages, which play a very important role in further exacerbating the disease [10]. Furthermore, histological images have shown that prior to the onset of complex plaque development in human tissues [11,12] and experimental models of atherosclerosis, markers of inflammation are observed in SMCs in the media of the vessel wall, such as VCAM-1 and inflammatory transcriptional mediators, such as activated NF-κB [13,14]. …”

Section: Discussionmentioning

confidence: 99%

C-reactive protein/oxidised low-density lipoprotein/β2-glycoprotein I complex promotes atherosclerosis in diabetic BALB/c mice via p38mitogen-activated protein kinase signal pathway

Zhang

Zhou

et al. 2013

Lipids Health Dis

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Section: Discussionmentioning

confidence: 99%

C-reactive protein/oxidised low-density lipoprotein/β2-glycoprotein I complex promotes atherosclerosis in diabetic BALB/c mice via p38mitogen-activated protein kinase signal pathway

Zhang

Zhou

et al. 2013

Lipids Health Dis

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“…1 a) [3] . Furthermore, histological images have shown that prior to the onset of complex plaque development in human tissues [4,5] and experimental models of atherosclerosis, markers of inflammation are observed in SMCs in the media of the vessel wall, such as VCAM-1 ( fig. 1 b, c, respectively) and inflammatory transcriptional mediators, such as activated NF-B [6,7] .…”

mentioning

confidence: 99%

Complex Regulation and Function of the Inflammatory Smooth Muscle Cell Phenotype in Atherosclerosis

et al. 2009

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“…Obviously, to reach an outer intimal layer, lipids are required to diffuse through numerous cell layers and a significant amount of matrix situated between the intimal cells. However, in diffusion or “filtration pressure” [106] models, the highest lipid accumulation must be most proximal to a lumen, diminishing proportionally to intimal depth, comparable to patterns of lipid accumulation in tunica intima of non-diseased human aortas of individuals aged 6–15 years [107]. Therefore, why does lipid accumulation in coronary atherosclerosis start in the deep layers of DIT, just above the internal elastic lamina, distant from the lumen?…”

Section: Discussionmentioning

confidence: 99%

“…It is known that such deposition occurs in normal aorta, although resulting in a different pattern [107]. However, in the author’s model, lipoprotein deposition from the arterial lumen becomes irrelevant.…”

Section: Discussionmentioning

confidence: 99%

Neovascularization of coronary tunica intima (DIT) is the cause of coronary atherosclerosis. Lipoproteins invade coronary intima via neovascularization from adventitial vasa vasorum, but not from the arterial lumen: a hypothesis

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2012

Theor Biol Med Model

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Background An accepted hypothesis states that coronary atherosclerosis (CA) is initiated by endothelial dysfunction due to inflammation and high levels of LDL-C, followed by deposition of lipids and macrophages from the luminal blood into the arterial intima, resulting in plaque formation. The success of statins in preventing CA promised much for extended protection and effective therapeutics. However, stalled progress in pharmaceutical treatment gives a good reason to review logical properties of the hypothesis underlining our efforts, and to reconsider whether our perception of CA is consistent with facts about the normal and diseased coronary artery. Analysis To begin with, it must be noted that the normal coronary intima is not a single-layer endothelium covering a thin acellular compartment, as claimed in most publications, but always appears as a multi-layer cellular compartment, or diffuse intimal thickening (DIT), in which cells are arranged in many layers. If low density lipoprotein cholesterol (LDL-C) invades the DIT from the coronary lumen, the initial depositions ought to be most proximal to blood, i.e. in the inner DIT. The facts show that the opposite is true, and lipids are initially deposited in the outer DIT. This contradiction is resolved by observing that the normal DIT is always avascular, receiving nutrients by diffusion from the lumen, whereas in CA the outer DIT is always neovascularized from adventitial vasa vasorum . The proteoglycan biglycan, confined to the outer DIT in both normal and diseased coronary arteries, has high binding capacity for LDL-C. However, the normal DIT is avascular and biglycan-LDL-C interactions are prevented by diffusion distance and LDL-C size (20 nm), whereas in CA, biglycan in the outer DIT can extract lipoproteins by direct contact with the blood. These facts lead to the single simplest explanation of all observations: (1) lipid deposition is initially localized in the outer DIT; (2) CA often develops at high blood LDL-C levels; (3) apparent CA can develop at lowered blood LDL-C levels. This mechanism is not unique to the coronary artery: for instance, the normally avascular cornea accumulates lipoproteins after neovascularization, resulting in lipid keratopathy. Hypothesis Neovascularization of the normally avascular coronary DIT by permeable vasculature from the adventitial vasa vasorum is the cause of LDL deposition and CA. DIT enlargement, seen in early CA and aging, causes hypoxia of the outer DIT and induces neovascularization. According to this alternative proposal, coronary atherosclerosis is not related to inflammation and can occur in individuals with normal circulating levels of LDL, consistent with research findings.

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Investigation of Sudan IV staining areas in aortas of infants and children: Possible prelesional stages of atherogenesis

Cited by 12 publications

References 35 publications

C-reactive protein/oxidised low-density lipoprotein/β2-glycoprotein I complex promotes atherosclerosis in diabetic BALB/c mice via p38mitogen-activated protein kinase signal pathway

C-reactive protein/oxidised low-density lipoprotein/β2-glycoprotein I complex promotes atherosclerosis in diabetic BALB/c mice via p38mitogen-activated protein kinase signal pathway

Complex Regulation and Function of the Inflammatory Smooth Muscle Cell Phenotype in Atherosclerosis

Neovascularization of coronary tunica intima (DIT) is the cause of coronary atherosclerosis. Lipoproteins invade coronary intima via neovascularization from adventitial vasa vasorum, but not from the arterial lumen: a hypothesis

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