Oxidized LDL and LOX-1 in experimental sepsis.
Oxidized LDL and LOX-1 in experimental sepsis.
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DOI：
10.1155/2013/761789
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发表时间：
2013
影响因子：
4.6
通讯作者：
Lehmann C
中科院分区：
文献类型：
--
作者：
Al-Banna N;Lehmann C
氧化低密度脂蛋白（oxLDL）和凝集素样oxLDL受体-1（LOX-1）在炎症中上调。由于炎症和毛细血管渗漏在微循环损伤中的重要性，这反过来又有助于脓毒症和多器官衰竭的发展，氧化LDL和LOX-1作为肠道炎症的参与者的作用引起了极大的兴趣。事实上，在实验性内毒素血症期间阻断LOX-1可有效降低白细胞活化。oxLDL参与局部和全身炎症的机制包括细胞增殖、细胞凋亡、毛细血管灌注、白细胞-内皮细胞相互作用和内皮细胞活化。这篇综述强调了oxLDL和LOX-1与促炎性疾病机制相关的证据。我们还指出，由于暴露时间，剂量或氧化程度，oxLDL参与疾病解决的情况。LOX-1反应的调节可用于治疗局部和全身炎症，但成功使用该靶标需要进一步了解其广泛的作用。
Oxidized low-density lipoproteins (oxLDL) and the lectin-like oxLDL receptor-1 (LOX-1) are upregulated in inflammation. Because of the importance of inflammation and capillary leakage in the impairment of the microcirculation, which in turn contributes to the development of sepsis and multiorgan failure, the role of oxidized LDL and LOX-1 as players of intestinal inflammation is of great interest. In fact, the blockade of LOX-1 during experimental endotoxemia was effective in reducing leukocyte activation. There are several mechanisms by which oxLDL can participate in local and systemic inflammation, including cell proliferation, apoptosis, capillary perfusion, leukocyte-endothelial cell interactions, and endothelial activation. This review highlights the evidence relating oxLDL and LOX-1 to proinflammatory disease mechanisms. We also indicate situations when oxLDL, because of exposure time, dose, or degree of oxidization, is involved in disease resolution. Modulation of LOX-1 response could be utilized for the treatment of local and systemic inflammation, but the successful use of this target requires further understanding of its broad effects.
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影响因子：
9.8
作者：
Katayama, T;Tanaka-Shiraishi, AT;Ito, M
通讯作者：
Ito, M
DOI：
10.1161/01.atv.18.10.1541
发表时间：
1998-10-01
影响因子：
8.7
作者：
Moriwaki, H;Kume, N;Kita, T
通讯作者：
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DOI：
10.1152/ajpheart.1996.271.5.h1795
发表时间：
1996-11-01
影响因子：
4.8
作者：
Liao, LX;Granger, DN
通讯作者：
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DOI：
10.1161/01.atv.15.12.2305
发表时间：
1995-12-01
影响因子：
8.7
作者：
LIAO, LX;AW, TY;GRANGER, DN
通讯作者：
GRANGER, DN
DOI：
10.1073/pnas.95.16.9535
发表时间：
1998-08-04
影响因子：
11.1
作者：
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通讯作者：
Masaki, T