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磷脂衍生的溶血磷脂在(病理)生理学中的作用。

Phospholipid-derived lysophospholipids in (patho)physiology.

机构信息

Institute of Medical Physics and Biophysics, Faculty of Medicine, Leipzig University, Härtelstr. 16-18, D 04107 Leipzig, Germany.

Institute of Medical Physics and Biophysics, Faculty of Medicine, Leipzig University, Härtelstr. 16-18, D 04107 Leipzig, Germany.

出版信息

Atherosclerosis. 2024 Nov;398:118569. doi: 10.1016/j.atherosclerosis.2024.118569. Epub 2024 Aug 23.

Abstract

Phospholipids (PL) are major components of cellular membranes and changes in PL metabolism have been associated with the pathogenesis of numerous diseases. Lysophosphatidylcholine (LPC) in particular, is a comparably abundant component of oxidatively damaged tissues. LPC originates from the cleavage of phosphatidylcholine (PC) by phospholipase A or the reaction of lipids with reactive oxygen species (ROS) such as HOCl. Another explanation of increased LPC concentration is the decreased re-acylation of LPC into PC. While there are also several other lysophospholipids, LPC is the most abundant lysophospholipid in mammals and will therefore be the focus of this review. LPC is involved in many physiological processes. It induces the migration of lymphocytes, fostering the production of pro-inflammatory compounds by inducing oxidative stress. LPC also "signals" via G protein-coupled and Toll-like receptors and has been implicated in the development of different diseases. However, LPCs are not purely "bad": this is reflected by the fact that the concentration and fatty acyl composition of LPC varies under different conditions, in plasma of healthy and diseased individuals, in tissues and different tumors. Targeting LPC and lipid metabolism and restoring homeostasis might be a potential therapeutic method for inflammation-related diseases.

摘要

磷脂(PL)是细胞膜的主要成分,PL 代谢的变化与许多疾病的发病机制有关。特别是溶血磷脂酰胆碱(LPC),是氧化损伤组织中相对丰富的成分。LPC 来源于磷脂酶 A 对磷脂酰胆碱(PC)的裂解,或者脂质与活性氧(ROS)如次氯酸(HOCl)的反应。LPC 浓度增加的另一个解释是 LPC 向 PC 的再酰化减少。虽然还有其他几种溶血磷脂,但 LPC 是哺乳动物中最丰富的溶血磷脂,因此将成为本综述的重点。LPC 参与许多生理过程。它诱导淋巴细胞迁移,通过诱导氧化应激促进促炎化合物的产生。LPC 还通过 G 蛋白偶联和 Toll 样受体“信号传递”,并与不同疾病的发展有关。然而,LPC 并不完全是“坏的”:这反映在 LPC 的浓度和脂肪酸组成在不同条件下变化的事实,在健康和患病个体的血浆中,在组织和不同肿瘤中。针对 LPC 和脂质代谢并恢复体内平衡可能是与炎症相关疾病的一种潜在治疗方法。

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