2018
DOI: 10.1016/j.lfs.2018.02.024
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LOX-1 receptor: A potential link in atherosclerosis and cancer

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Cited by 114 publications
(92 citation statements)
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“…These markers promote the influx and activation of other inflammatory cells, as T‐lymphocytes, and mediate their retention in the plaque that increases the inflammatory process around it . Besides that, the NO induces high production of peroxynitrite and consequent cell toxicity …”
Section: Discussionsupporting
confidence: 81%
See 1 more Smart Citation
“…These markers promote the influx and activation of other inflammatory cells, as T‐lymphocytes, and mediate their retention in the plaque that increases the inflammatory process around it . Besides that, the NO induces high production of peroxynitrite and consequent cell toxicity …”
Section: Discussionsupporting
confidence: 81%
“…[60,61] Besides that, the NO induces high production of peroxynitrite and consequent cell toxicity. [62] DTP and digested glutelin were the most effective to reduce the expression of NF-κB and iNOS, and the secretion of TNF-α, PGE-2, MCP-1, and IL-6, which are the inflammatory markers in the atherosclerosis process. These results showed the effectiveness of digested protein from chia seed, like others studies with bean hydrolysates [43] and extruded amaranth hydrolysate.…”
Section: Discussionmentioning
confidence: 98%
“…However, above the dose of 10 ng/mL, TNF-α reduced about 10% of cell viability (Figure 1a). Because MMPs break down components of ECM, which is a crucial role in the process of VSMC migration [7,8], the effect of TNF-α on MMP activities was then tested by gelatin zymography in serum-free conditioned medium to identify the contribution of MMP-2 or MMP-9 to the pro-migratory ability of TNF-α. As shown in Figure 1b, MMP-9 activity was tremendously increased by TNF-α in a concentration-dependent manner, whereas MMP-2 activity was less affected.…”
Section: Non-cytotoxic Doses Of Hlp Inhibits Tnf-α-induced Cell Viabimentioning
confidence: 99%
“…A constitutive expression of LOX-1 is observed in vascular endothelial cells in the physiological state. In addition, macrophages and platelets show inducible LOX-1 expression stimulated by inflammatory cytokines as a result of ischemia and vascular injury [18]. The binding of several ligands to LOX-1 induces superoxide generation, inhibits NO production, and enhances the endothelial adhesiveness of leukocytes.…”
Section: Discussionmentioning
confidence: 99%