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视网膜缺血再灌注损伤可引起强烈的脂质合成和重塑。

Retinal ischemia-reperfusion injury induces intense lipid synthesis and remodeling.

机构信息

Department of Ophthalmology, Peking University Third Hospital, Beijing, 100191, China; Beijing Key Laboratory of Restoration of Damaged Ocular Nerve, Peking University Third Hospital, Beijing, 100191, China.

Department of Ophthalmology, The Fifth Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, Henan, China.

出版信息

Biochem Biophys Res Commun. 2023 Dec 31;689:149232. doi: 10.1016/j.bbrc.2023.149232. Epub 2023 Nov 10.

Abstract

The retina is a high-metabolism tissue composed of various cell types with complex functions that relies heavily on the blood supply to maintain homeostasis. Retinal ischemia-reperfusion injury is a critical pathogenic mechanism in glaucoma, and changes in lipid molecules may lead to retinal tissue damage. However, retinal lipid profile alterations caused by this mechanism remain unclear. Thus, this study employed a retinal ischemia-reperfusion model to analyze changes in the lipid profile between sham-operated and ischemia-reperfusion groups. We discovered that ischemia-reperfusion injury-induced alterations in 338 lipid molecules, which potentially caused lipid droplet formation and mitochondrial damage. Notably, we identified characteristic changes in various lipids, including cholesterol esters, cardiolipin, and ceramide, which may serve as potential biomarkers for assessing the severity of retinal injury and therapeutic interventions. The ischemia-reperfusion-specific features identified in this study provide a more comprehensive understanding of the pathophysiological mechanisms underlying this condition.

摘要

视网膜是一种新陈代谢旺盛的组织,由具有复杂功能的各种细胞类型组成,严重依赖血液供应来维持其体内平衡。视网膜缺血再灌注损伤是青光眼的一个关键致病机制,脂质分子的变化可能导致视网膜组织损伤。然而,这种机制引起的视网膜脂质谱改变尚不清楚。因此,本研究采用视网膜缺血再灌注模型分析了假手术组和缺血再灌注组之间的脂质谱变化。我们发现,缺血再灌注损伤诱导了 338 种脂质分子的改变,这可能导致脂滴形成和线粒体损伤。值得注意的是,我们鉴定了各种脂质的特征性变化,包括胆固醇酯、心磷脂和神经酰胺,它们可能作为评估视网膜损伤严重程度和治疗干预的潜在生物标志物。本研究中确定的缺血再灌注特异性特征提供了对该疾病病理生理机制的更全面理解。

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