Oxidative lipidomics: applications in critical care

Abstract

Purpose of the review Lipid peroxidation has long been established as a key player in the pathophysiology of critical care illnesses. Recent developments in oxidative lipidomics have aided in deciphering the molecular mechanisms of lipid oxidation. This review discusses the achievements and recent developments of oxidative lipidomics and its contribution to the understanding of critical illness. Recent findings Most studies involving acute injury focus on identifying the end products of lipid peroxidation. This misses the early events and targets of peroxidation mechanisms. Recent developments in LC-MS based oxidative lipidomics have enabled the identification of a wide variety of enzymatically generated lipid oxidation products both in clinical as well as animal injury models. Such lipid mediators have been found to play an important role in injury, inflammation, and recovery in disease states such as sepsis or head trauma. Summary Oxidative stress produces multiple lipid oxidation products either through enzymatic pathways or through free radical reactions. These products are often biologically active and can contribute to the regulation of cellular signaling. Oxidative lipidomics has contributed to the understanding of lipid peroxidation products, the mechanism of their production, time course of development after injury, and synergistic functioning with other regulatory processes in the body. These advances in knowledge will help guide the future development of interventions in critical illness.

Pathophysiology, echocardiographic evaluation, biomarker findings, and prognostic implications of septic cardiomyopathy: a review of the literature

“…These molecules, acting through varied signal transduction pathways, which in some cases alter gene expression, activate both positive and negative feedback loops within the immune system [ 12 ]. Recent advances in oxidative lipidomics have identified products of upstream lipid metabolism that are involved in the initiation (eicosanoids) and recovery phases (lipoxins, resolvins) [ 13 ]. Sepsis-induced dysregulation of the normal immune response can lead to a variety of deleterious effects, including SC, multi-system organ failure, and ultimately death in some patients [ 5 ] .…”

Oxidized phospholipid signaling in traumatic brain injury

“…Through advances in HPLC and mass spectrometry-based oxidative lipidomics, hydroperoxy lipid species can now be detected and quantified [38, 48, 51, 67]. The advent of oxidative lipidomics [68] has begun to reveal the diversity of lipid oxidation after TBI and elucidate enzymatic mechanisms of lipid oxidation that could potentially be targeted. Understanding the source and signaling associated with lipid oxidation is important in therapeutic targeting and may explain why general antioxidative treatment strategies have so far failed in clinical translation.…”

“…In line with its role in the clearance of apoptotic cells, PS oxidation occurs only by 24 hr. Efferocytosis serves a critical role in modulating the inflammatory response and promoting injury resolution [67, 68]. Importantly another lipid mediator implicated in resolution of inflammation, resolvins, are also pronounced during this time, indicating synergetic effects of oxidized lipid mediators in the resolution of inflammation.…”

Role of TXNIP/NLRP3 in sepsis-induced myocardial dysfunction

“…The overactivation of apoptosis is an important pathological feature of tissue damage during sepsis (5), however, the specific mechanism underlying the tissue damage and excessive apoptosis of cells remains to be fully elucidated. The close association between the oxidative stress response and inflammation has received increasing attention in recent years, and the effects of inflammation on mitochondrial function lead to an increase in the production of reactive oxygen species (ROS), which in turn causes tissue damage through the activation of oxidative stress (6).…”