Li Pin-Lan, Gulbins Erich
Department of Pharmacology and Toxicology, School of Medicine, Virginia Commonwealth University, Richmond, Virginia.
Institute of Molecular Biology, University of Duisburg-Essen, Essen, Germany.
Antioxid Redox Signal. 2018 Apr 1;28(10):911-915. doi: 10.1089/ars.2017.7467. Epub 2018 Jan 24.
The actions of bioactive lipids and reactive oxygen species (ROS) are usually coupled, and their interplay is a common and important mechanism mediating tissue injury, inflammation, and other pathologies. Understanding the interplay of ROS and lipid mediators will extend horizons for researchers to clarify the pathogenesis of different diseases and help identify therapeutic targets for treatment of these diseases. Some bioactive lipids are converted into oxidized lipids during cell or tissue oxidative stress such as isoprostanes and isoketals, which are even more bioactive than their precursors. Moreover, many enzymes that produce lipid mediators such as prostaglandin H synthases, lipoxygenases, and cytochrome P450 isoforms may catalyze the production of ROS. Bioactive lipids-lysophospholipids, sphingolipids, or deposited lipids in cells-are shown to stimulate redox enzymes to produce ROS. In addition, a lipid-channel-ROS axis in different organelles may be associated with the crosstalk of ROS and bioactive lipids. This Forum focuses on the crosstalk of ROS with sphingolipids, P450 eicosanoids, lysophospholipids, and deposited plasma lipids and related novel signaling pathway in their reciprocal actions, which is expected to provide novel insights into the pathogenesis of different diseases associated with the participation of these lipid mediators. It is imperative to further understand the molecular mechanism mediating the crosstalk of ROS with specific lipid mediators and to develop more effective therapeutic strategies to target the interplay of ROS and lipid mediators for treatment specific to different organ diseases. . 28, 911-915.
生物活性脂质与活性氧(ROS)的作用通常相互关联,它们之间的相互作用是介导组织损伤、炎症及其他病理过程的常见且重要的机制。了解ROS与脂质介质之间的相互作用将拓宽研究人员阐明不同疾病发病机制的视野,并有助于确定治疗这些疾病的靶点。在细胞或组织氧化应激过程中,一些生物活性脂质会转化为氧化脂质,如异前列腺素和异酮醛,它们比其前体更具生物活性。此外,许多产生脂质介质的酶,如前列腺素H合成酶、脂氧合酶和细胞色素P450同工型,可能催化ROS的产生。生物活性脂质——溶血磷脂、鞘脂或细胞内沉积的脂质——已被证明可刺激氧化还原酶产生ROS。此外,不同细胞器中的脂质通道-ROS轴可能与ROS和生物活性脂质的相互作用有关。本论坛聚焦于ROS与鞘脂、P450类二十烷酸、溶血磷脂及沉积的血浆脂质之间的相互作用以及它们相互作用中的相关新信号通路,有望为这些脂质介质参与的不同疾病的发病机制提供新见解。进一步了解介导ROS与特定脂质介质相互作用的分子机制,并开发更有效的治疗策略以针对ROS与脂质介质的相互作用来治疗不同器官疾病势在必行。 28, 911 - 915。