Shock, Trauma and Anesthesiology Research (STAR) Center, Department of Anesthesiology, Baltimore, MD, 21201, USA.
Shock, Trauma and Anesthesiology Research (STAR) Center, Department of Anesthesiology, Baltimore, MD, 21201, USA; Department of Anatomy and Neurobiology, University of Maryland School of Medicine, Baltimore, MD, 21201, USA.
Neurochem Int. 2024 May;175:105701. doi: 10.1016/j.neuint.2024.105701. Epub 2024 Feb 28.
Brain tissue is highly enriched in lipids, the majority of which are glycerophospholipids. Glycerophospholipids are the major constituents of cellular membranes and play an important role in maintaining integrity and function of cellular and subcellular structures. Any changes in glycerophospholipid homeostasis can adversely affect brain functions. Traumatic brain injury (TBI), an acquired injury caused by the impact of external forces to the brain, triggers activation of secondary biochemical events that include perturbation of lipid homeostasis. Several studies have demonstrated glycerophospholipid dysregulation in the brain and circulation after TBI. This includes spatial and temporal changes in abundance and distribution of glycerophospholipids in the injured brain. This is at least in part mediated by TBI-induced oxidative stress and by activation of lipid metabolism pathways involved in tissue repairing. In this review, we discuss current advances in understanding of the mechanisms and implications of glycerophospholipid dysregulation following TBI.
脑组织富含脂质，其中大部分为甘油磷脂。甘油磷脂是细胞膜的主要成分，在维持细胞和亚细胞结构的完整性和功能方面发挥着重要作用。甘油磷脂稳态的任何变化都可能对大脑功能产生不利影响。创伤性脑损伤（TBI）是一种由外力对大脑造成的获得性损伤，会引发继发性生化事件的激活，包括脂质稳态的紊乱。几项研究表明，TBI 后大脑和循环中的甘油磷脂发生失调。这包括损伤大脑中甘油磷脂丰度和分布的时空变化。这至少部分是由 TBI 诱导的氧化应激和参与组织修复的脂质代谢途径的激活所介导的。在这篇综述中，我们讨论了目前对 TBI 后甘油磷脂失调的机制和影响的理解进展。
