Abstract
Globally, traumatic brain injury (TBI) is an acute clinical event and an important cause of death and long-term disability. However, the underlying mechanism of the pathophysiological has not been fully elucidated and the lack of effective treatment a huge burden to individuals, families, and society. Several studies have shown that long non-coding RNAs (lncRNAs) might play a crucial role in TBI; they are abundant in the central nervous system (CNS) and participate in a variety of pathophysiological processes, including oxidative stress, inflammation, apoptosis, blood-brain barrier protection, angiogenesis, and neurogenesis. Some lncRNAs modulate multiple therapeutic targets after TBI, including inflammation, thus, these lncRNAs have tremendous therapeutic potential for TBI, as they are promising biomarkers for TBI diagnosis, treatment, and prognosis prediction. This review discusses the differential expression of different lncRNAs in brain tissue during TBI, which is likely related to the physiological and pathological processes involved in TBI. These findings may provide new targets for further scientific research on the molecular mechanisms of TBI and potential therapeutic interventions.
Highlights
Traumatic Brain Injury (TBI) is the direct or indirect effect of external force on the head, causing mechanical damage to the brain tissue, and a series of secondary pathological injuries
LncRNAs are involved in various biological processes, including signal transduction, immune response, inflammatory pathways, ion channel regulation, and cell cycle
Previous studies have reported that long non-coding RNAs (lncRNAs) are differentially expressed in the brain tissue after TBI and that they mediate the pathophysiological process of inflammation in TBI
Summary
Traumatic Brain Injury (TBI) is the direct or indirect effect of external force on the head, causing mechanical damage to the brain tissue, and a series of secondary pathological injuries. Various lncRNAs, such as NEAT1, MALAT1, maternally expressed gene 3 (MEG3), and growth arrest-specific transcript 5 (GAS5) regulate inflammatory pathways and immune responses that mediate apoptosis in neuronal cells (Zhang and Wang, 2019).
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