atherogenesis


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Related to atherogenesis: dyslipidemia

atherogenesis

 [ath″er-o-jen´ĕ-sis]
formation of abnormal fatty or lipid masses in arterial walls. adj., adj atherogen´ic.

ath·er·o·gen·e·sis

(ath'er-ō-jen'ĕ-sis),
Formation of atheroma, important in the pathogenesis of arteriosclerosis.

atherogenesis

(ăth′ər-ō-jĕn′ĭ-sĭs)
n.
Formation of atheromatous deposits, especially on the innermost layer of arterial walls.

ath′er·o·gen′ic (-jĕn′ĭk) adj.
ath′er·o·gen·i′ci·ty (-jə-nĭs′ĭ-tē) n.

ath·er·o·gen·e·sis

(ath'ĕr-ō-jen'ĕ-sis)
Formation of atheroma, important in the pathogenesis of arteriosclerosis.
References in periodicals archive ?
Inflammation at the Molecular Interface of Atherogenesis: An Anthropological Journey.
Despite increasing evidence that LOX-1, a cell-surface receptor for oxLDL, is implicated in thrombogenesis and atherogenesis, its involvement in the regulation of TF expression in macrophages remains unclear.
pylori infection and chronic progression of atherogenesis; but the mechanism is not identified perfectly yet [2].
This is based on the hypothesis that inhibits LDL oxidation, thereby protecting against atherogenesis. In addition, tocopherols inhibit platelet aggregation and thrombogenesis [29].
The association between viral steatosis and atherogenesis acceleration has not been studied yet.
Heinecke, "Thematic review series: the immune system and atherogenesis. Lipoprotein-associated inflammatory proteins: markers or mediators of cardiovascular disease?," Journal of Lipid Research, vol.
Although VSMC proliferation is beneficial throughout atherogenesis by having a reparative effect, VSMC cell death and senescence promote both atherogenesis and multiple features of plaque instability.
It is very likely that this pool of [Mn.sup.2+] is formed as a result of the high-rate disintegration of the AP cells during atherogenesis. This pool of extracellular [Mn.sup.2+], available in structures of the tissue matrix, could grow with the degree of the instability of AP which is accompanied by active cell death and disintegration.
Our previous studies showed that the expression level of miR-106b-5p was upregulated in the plasma of patients with unstable atherosclerotic plaques,[sup][9] which might be derived from microparticles released by the systemically activated/apoptotic ECs.[sup][9],[10] Besides, by predicting the possible target genes of miR-106b-5p with bioinformatics analysis, we found that miR-106b-5p may involve in several aspects of atherosclerosis, such as inflammation, angiogenesis, apoptosis, and extracellular matrix (ECM) degradation.[sup][9] However, the exact mechanism(s) underlying miR-106b-5p in the atherogenesis remain(s) poorly understood.
These preventive measures, however, are indirect, as they are aimed to alter certain conditions, which are not immediately related to the molecular and cellular mechanisms of atherogenesis. Another therapeutic strategy implicates a "direct" therapy, which is aimed to prevent the onset and progression of atherosclerotic lesions by inhibiting the molecular and cellular mechanisms of atherogenesis in human arteries (Orekhov and Tertov 1997; Orekhov et al.
Neopterin stimulates nuclear factor-kB translocation to the nucleus promoting the expression of proinflammatory genes, adhesion molecules, tissue factor, and other substances implicated in the inflammatory processes that take place within the arterial wall in atherogenesis and atheromatous plaque disruption.