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Review
. 2024 May:175:105701.
doi: 10.1016/j.neuint.2024.105701. Epub 2024 Feb 28.

Glycerophospholipid dysregulation after traumatic brain injury

Chinmoy Sarkar  1 , Marta M Lipinski  2
Affiliations
Review

Glycerophospholipid dysregulation after traumatic brain injury

Chinmoy Sarkar et al. Neurochem Int. 2024 May.

Abstract

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.

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Conflict of interest statement

Declaration of competing interest This work was supported by NIH R21 (R21NS117867) grant to CS and NIH R01 (R01 NS115876) to MML.

Figures

Figure 1.
Figure 1.
Schematic diagram representing cellular mechanisms of phospholipid dysregulation after TBI. PL – Phospholipids; LPL – Lyso-PLs; PLA2 – Phospholipase A2; ROS – Reactive oxygen species. This figure was created with Biorender.com.
See this image and copyright information in PMC

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