髓系ACAT1/SOAT1:血脂异常和视网膜新生血管的新调节因子。

Syed A H Zaidi, Ruth B Caldwell, Modesto A Rojas
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引用次数: 0

摘要

病理性视网膜新生血管(RNV)是缺血性视网膜病变期间视力丧失和失明的主要原因。我们对氧致视网膜病变(OIR)小鼠模型的研究揭示了一种新的病理RNV和神经血管损伤机制。我们发现,oir诱导的巨噬细胞/小胶质细胞的激活、视网膜炎症和病理性RNV是由酰基辅酶a:胆固醇酰基转移酶1/甾醇o -酰基转移酶1 (ACAT1/SOAT1)酶的激活导致胆固醇酯(CE)形成的增加介导的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Myeloid ACAT1/SOAT1: a novel regulator of dyslipidemia and retinal neovascularization.

Pathological retinal neovascularization (RNV) is a major cause of vision loss and blindness during ischemic retinopathies. Our investigations in the mouse model of oxygen-induced retinopathy (OIR) demonstrate a novel mechanism of pathological RNV and neurovascular injury. We show that OIR-induced activation of macrophage/microglial cells, retinal inflammation, and pathological RNV are mediated by increases in cholesterol ester (CE) formation due to activation of the acyl-CoA: Cholesterol Acyltransferase 1/Sterol O-Acyltransferase 1 (ACAT1/SOAT1) enzyme.

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