The Role of Lipoproteins in Human Atherosclerosis (Lecture I)

1978 ◽  
pp. 237-244
Author(s):  
K. W. Walton
Keyword(s):  
Human Atherosclerosis

scholarly journals The Role of Monocytes and Macrophages in Human Atherosclerosis, Plaque Neoangiogenesis, and Atherothrombosis

2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Francesco Moroni ◽  
Enrico Ammirati ◽  
Giuseppe Danilo Norata ◽  
Marco Magnoni ◽  
Paolo G. Camici
Keyword(s):  
Animal Studies ◽  
Arterial Wall ◽  
Causes Of Death ◽  
Complex Disease ◽  
Potential Role ◽  
Innate Immune ◽  
Pathogenic Role ◽  
Monocytes And Macrophages ◽  
Human Atherosclerosis

Atherosclerosis is one of the leading causes of death and disability worldwide. It is a complex disease characterized by lipid accumulation within the arterial wall, inflammation, local neoangiogenesis, and apoptosis. Innate immune effectors, in particular monocytes and macrophages, play a pivotal role in atherosclerosis initiation and progression. Although most of available evidence on the role of monocytes and macrophages in atherosclerosis is derived from animal studies, a growing body of evidence elucidating the role of these mononuclear cell subtypes in human atherosclerosis is currently accumulating. A novel pathogenic role of monocytes and macrophages in terms of atherosclerosis initiation and progression, in particular concerning the role of these cell subsets in neovascularization, has been discovered. The aim of the present article is to review currently available evidence on the role of monocytes and macrophages in human atherosclerosis and in relation to plaque characteristics, such as plaque neoangiogenesis, and patients’ prognosis and their potential role as biomarkers.

Cellular mechanisms of human atherosclerosis: Role of cell-to-cell communications in subendothelial cell functions

2016 ◽  
Vol 48 (1) ◽  
pp. 25-34 ◽  
Author(s):  
Alexander N. Orekhov ◽  
Elena R. Andreeva ◽  
Yuri V. Bobryshev
Keyword(s):  
Cellular Mechanisms ◽  
Cell Functions ◽  
Human Atherosclerosis

The role of macrophages and giant cells in advanced human atherosclerosis

1980 ◽  
Vol 36 (3) ◽  
pp. 441-447 ◽  
Author(s):  
O.B. Bayliss High ◽  
C.W.M. Adams
Keyword(s):  
Giant Cells ◽  
Human Atherosclerosis

Expression and function of ephrin-B1 and its cognate receptor EphB2 in human atherosclerosis: from an aspect of chemotaxis

2008 ◽  
Vol 114 (10) ◽  
pp. 643-650 ◽  
Author(s):  
Aiji Sakamoto ◽  
Hatsue Ishibashi-Ueda ◽  
Yuka Sugamoto ◽  
Takeo Higashikata ◽  
Susumu Miyamoto ◽  
...  
Keyword(s):  
T Lymphocytes ◽  
Cdna Array ◽  
Monocyte Chemoattractant Protein 1 ◽  
Reverse Transcription Pcr ◽  
Cytokines And Chemokines ◽  
Human Atherosclerosis ◽  
And Function ◽  
Arterial Endothelial Cells ◽  
Human Carotid

Although several cytokines and chemokines have been demonstrated to play pivotal roles in the pathophysiological conditions of atherosclerosis, few findings exist regarding the expression and function of cytokine-modulating molecules such as ephrin-Bs and their cognate receptors, EphBs, in human atherosclerosis. Therefore, in the present study, we screened novel genes modulating atherogenesis by cDNA array and quantitatively determined them by real-time RT (reverse transcription)-PCR in human carotid atherosclerotic plaques. Ephrin-B1 and EphB2, key regulators of embryogenesis, were significantly up-regulated in plaques compared with those in adjacent control tissues [ephrin-B1, 0.638±0.106 compared with 0.831±0.152, or 130% (P<0.05); EphB2, 1.296±0.281 compared with 2.233±0.506, or 172% (P<0.05)]. Immunohistological analysis demonstrated that both ephrin-B1 and EphB2 were expressed in macrophages and T-lymphocytes in plaques as well as in monocytes, T-lymphocytes and arterial endothelial cells isolated from healthy adults. Interestingly, the extracellular domains of ephrin-B1 and EphB2, the expression of which were both enhanced in stimulated THP-1 cells, significantly inhibited spontaneous (22.5 and 27.6% respectively; P<0.01) and MCP-1 (monocyte chemoattractant protein-1)-dependent (29.7 and 22.6% respectively; P<0.01) migration of monocytes. In conclusion, these results demonstrate that ephrin-B1 and EphB2 are overexpressed in atherosclerotic tissue and might locally regulate cell migration, possibly through modulating cytokine-related chemotaxic activity; however, the functional role of these molecules in atherogenesis should be investigated further.

scholarly journals Role of Asymmetrical Dimethylarginine in Inflammation-Induced Endothelial Dysfunction in Human Atherosclerosis

Hypertension ◽  
2011 ◽  
Vol 58 (1) ◽  
pp. 93-98 ◽  
Author(s):  
Charalambos Antoniades ◽  
Michael Demosthenous ◽  
Dimitris Tousoulis ◽  
Alexios S. Antonopoulos ◽  
Charalambos Vlachopoulos ◽  
...  
Keyword(s):  
Endothelial Dysfunction ◽  
Asymmetrical Dimethylarginine ◽  
Human Atherosclerosis

scholarly journals Monocyte-chemoattractant protein-1 Levels in Human Atherosclerosis Associate with Plaque Vulnerability

2020 ◽  
Author(s):  
Marios K Georgakis ◽  
Sander W. van der Laan ◽  
Yaw Asare ◽  
Joost M. Mekke ◽  
Saskia Haitjema ◽  
...  
Keyword(s):  
Intraplaque Hemorrhage ◽  
Vascular Risk ◽  
Plaque Vulnerability ◽  
Monocyte Chemoattractant Protein 1 ◽  
Plaque Instability ◽  
Monocyte Chemoattractant ◽  
Monocyte Chemoattractant Protein ◽  
Human Atherosclerosis ◽  
Plaque Inflammation

Monocyte chemoattractant protein-1 (MCP-1) recruits monocytes to the atherosclerotic plaque. While experimental, genetic, and observational data support a key role of MCP-1 in atherosclerosis, the translational potential of targeting MCP-1 signaling for lowering vascular risk is limited by the lack of data on plaque MCP-1 activity in human atherosclerosis. Here, we measured MCP-1 levels in human plaque samples from 1,199 patients undergoing carotid endarterectomy and explored associations with histopathological, molecular, and clinical features of plaque vulnerability. MCP-1 plaque levels were associated with histopathological hallmarks of plaque vulnerability (large lipid core, low collagen, high macrophage burden, low smooth muscle cell burden, intraplaque hemorrhage) as well as with molecular markers of plaque inflammation and matrix turnover, clinical plaque instability, and periprocedural stroke during plaque removal. Collectively, our findings highlight a role of MCP-1 in human plaque vulnerability and suggest that interfering with MCP-1 signaling in patients with established atherosclerosis could lower vascular risk.

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