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JAK-STAT-dependent regulation of scavenger receptors in LPS-activated murine macrophages

机译:jak-stat依赖于LPS激活鼠巨噬细胞清除剂的调节

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摘要

In atherosclerosis progression, atherosclerotic plaques develop upon accumulated foam cells derived from macrophages that take up modified low-density lipoprotein (LDL). CD36 and CD204 are the principal scavenger receptors responsible for the uptake of modified LDL. Lipopolysaccharide (LPS) exacerbates atherosclerosis by enhancing the expression of scavenger receptors and thus increasing the uptake of modified LDL into macrophages. However, the signaling pathways that mediate LPS and scavenger receptor expression have not been fully elucidated.
机译:在动脉粥样硬化进展中,动脉粥样硬化斑块在衍生自巨噬细胞的累积泡沫细胞上产生血液凋亡,所述巨噬细胞凋亡的血液化脂肪蛋白(LDL)。 CD36和CD204是负责改性LDL的摄取的主要清除剂受体。 通过增强清除剂受体的表达并因此增加改性LDL进入巨噬细胞的吸收来加剧动脉粥样硬化。 然而,介导LPS和清除剂受体表达的信号传导途径尚未完全阐明。

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