Oxidized phospholipid signaling in traumatic brain injury
Anthonymuthu T. S., Kenny E. M., Lamade A. M., Kagan V. E., Bayır H.
Free Radical Biology & Medicine
Vol.124, P. 493-503
Опубликовано: 2018
Тип ресурса: Обзор
DOI:10.1016/j.freeradbiomed.2018.06.031
Аннотация:
Oxidative stress is a major contributor to secondary injury signaling cascades following traumatic brain injury (TBI). The role of lipid peroxidation in the pathophysiology of a traumatic insult to neural tissue is increasingly recognized. As the methods to quantify lipid peroxidation have gradually improved, so has the understanding of mechanistic details of lipid peroxidation and related signaling events in the injury pathogenesis. While free-radical mediated, non-enzymatic lipid peroxidation has long been studied, recent advances in redox lipidomics have demonstrated the significant contribution of enzymatic lipid peroxidation to TBI pathogenesis. Complex interactions between inflammation, phospholipid peroxidation, and hydrolysis define the engagement of different cell death programs and the severity of injury and outcome. This review focuses on enzymatic phospholipid peroxidation after TBI, including the mechanism of production, signaling roles in secondary injury pathology, and t
Ключевые слова:
Apoptosis; Efferocytosis; Ferroptosis; Inflammation; Lipid mediator; Redox lipidomics
cardiolipin; fatty acid; oxidized phospholipid; phosphatidylethanolamine; phosphatidylserine; phospholipid; unclassified drug; phospholipid; cellular distribution; disease severity; human; hydrolysis; inflammation; lipid peroxidation; lipidomics; nonhuman; oxidative stress; pathogenesis; pathophysiology; priority journal; Review; signal transduction; traumatic brain injury; animal; metabolism; oxidation reduction reaction; physiology; signal transduction; traumatic brain injury; Animals; Brain Injuries, Traumatic; Humans; Lipid Peroxidation; Oxidation-Reduction; Oxidative Stress; Phospholipids; Signal Transduction
Язык текста: Английский
ISSN: 1873-4596
Anthonymuthu T. S.
Kenny E. M.
Lamade A. M.
Kagan V. E. Valerian E 1946-
Bayır H.
Антхонyмутху Т. С.
Кеннy Е. М.
Ламаде А. М.
Каган В. Е. Валериан Е 1946-
Байıр Х.
Oxidized phospholipid signaling in traumatic brain injury
Текст визуальный непосредственный
Free Radical Biology & Medicine
Elsevier Science Publisher B.V.
Vol.124 P. 493-503
2018
Обзор
Apoptosis Efferocytosis Ferroptosis Inflammation Lipid mediator Redox lipidomics
cardiolipin fatty acid oxidized phospholipid phosphatidylethanolamine phosphatidylserine phospholipid unclassified drug phospholipid cellular distribution disease severity human hydrolysis inflammation lipid peroxidation lipidomics nonhuman oxidative stress pathogenesis pathophysiology priority journal Review signal transduction traumatic brain injury animal metabolism oxidation reduction reaction physiology signal transduction traumatic brain injury Animals Brain Injuries, Traumatic Humans Lipid Peroxidation Oxidation-Reduction Oxidative Stress Phospholipids Signal Transduction
Oxidative stress is a major contributor to secondary injury signaling cascades following traumatic brain injury (TBI). The role of lipid peroxidation in the pathophysiology of a traumatic insult to neural tissue is increasingly recognized. As the methods to quantify lipid peroxidation have gradually improved, so has the understanding of mechanistic details of lipid peroxidation and related signaling events in the injury pathogenesis. While free-radical mediated, non-enzymatic lipid peroxidation has long been studied, recent advances in redox lipidomics have demonstrated the significant contribution of enzymatic lipid peroxidation to TBI pathogenesis. Complex interactions between inflammation, phospholipid peroxidation, and hydrolysis define the engagement of different cell death programs and the severity of injury and outcome. This review focuses on enzymatic phospholipid peroxidation after TBI, including the mechanism of production, signaling roles in secondary injury pathology, and t