Status
Please wait ...

Details for phenotype: atherosclerosis

EndoNet ID: ENP00044

Name

atherosclerosis

General information

This phenotype is pathologic
  • Atherosclerosis is a common disorder that specifically affects the medium and large arteries. It occurs when fat, cholesterol, and other substances build up in the walls of arteries and form hard structures called plaques. [1]

Links to other resources

GO
Medline Plus 000171
MeSH term D050197
Disease database 1039

Phenotype triggers

  • more activity (high ligand concentration, overexpression) of Lysophosphatidic acid receptor 1
    in platelet
    • The effect of LPA on platelets may be species-specific, because LPA was found to inhibit platelet activation in mice. [2]
    • LPA has been implicated in the development of atherosclerosis during early (barrier dysfunction and monocyte adhesion of the endothelium) and later phases (platelet activation and thrombosis). [3]
    • LPA was found to accumulate in the thrombogenic lipid-rich core of atherosclerotic plaques. Pharmacological studies identified LPA1 as primary mediator of LPA-induced platelet activation. [4]
  • normal activity of Probable G-protein coupled receptor 132
    in macrophage
    • The key role of LPC as a major antigenic component of oxLDL has implicated this bioactive lipid in atherosclerosis, the primary cause of heart disease and stroke. [5]
    • Aspects of immune function as potential targets of LPC action play some role in atherogenesis. Macrophage responses to oxLDL such as migration and activation are likely determined to a significant extent by its LPC content, and may therefore be mediated to some degree via G2A and/or GPR4. [5]
  • normal activity of G-protein coupled receptor 4
    in macrophage
    • The key role of LPC as a major antigenic component of oxLDL has implicated this bioactive lipid in atherosclerosis, the primary cause of heart disease and stroke. [5]
    • Aspects of immune function as potential targets of LPC action play some role in atherogenesis. Macrophage responses to oxLDL such as migration and activation are likely determined to a significant extent by its LPC content, and may therefore be mediated to some degree via G2A and/or GPR4. [5]
  • more activity (high ligand concentration, overexpression) of mineralcorticoid receptor
    in macrophage
    • Aldosterone treatment increases oxidative stress in macrophages derived from ApoE-deficient mice. [6]
    • Aldosterone activation of MR in endothelial cells specifically modulates ICAM-1 expression and promotes leukocyte adhesion, supporting a role for MR signalling in endothelial cells in the initial stages of atherosclerosis. These findings highlight a key role for both macrophage and endothelial MR signalling in atherosclerosis. [7]
  • more activity (high ligand concentration, overexpression) of glucocorticoid receptor
    in macrophage
    • Atherosclerosis is a progressive disease characterised by an inflammatory event in which monocyte-derived macrophages play a central role. [8]
    • Glucocorticoid treatment has been shown to reduce macrophage accumulation in a model of cholesterol-induced atherosclerosis. [9]
    • Glucocorticoid treatment has been shown to decrease neointimal proliferation following balloon angioplasty. [10]
    • Effects of glucocorticoids on etiology and progression of atherosclerosis are only partially mediated through GR. [11]
  • more activity (high ligand concentration, overexpression) of TNFR1
    in bone_marrow
    • In atherosclerosis, TNF considered to promote plaque growth and progression. [12]
    • Bone-marrow derived p55 TNFR promotes atherosclerosis development by enhancing lesional foam-cell formation and by promoting expression of pro-atherosclerotic chemokines, like MCP-1. [13]
  • more activity (high ligand concentration, overexpression) of Lysophosphatidic acid receptor 3
    in platelet
    • LPA has been implicated in the development of atherosclerosis during early (barrier dysfunction and monocyte adhesion of the endothelium) and later phases (platelet activation and thrombosis). [3]
    • LPA was found to accumulate in the thrombogenic lipid-rich core of atherosclerotic plaques. Pharmacological studies identified LPA3 as primary mediator of LPA-induced platelet activation. [4]
    • The effect of LPA on platelets may be species-specific, because LPA was found to inhibit platelet activation in mice. [2]
Reference