Research Progress on the Inflammatory Effects of Long Non-coding RNA in Traumatic Brain Injury

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.

Keywords: immune response; inflammatory pathways; long non-coding RNA; therapy; traumatic brain injury.

FIGURE 1

Overview of long non-coding RNA (lncRNA) biogenesis. A Schematic diagram illustrating the origin of lncRNAs. (a), Intron sense or antisense lncRNAs. (b), Exon sense- or antisense lncRNAs. (c), between genes. (d), Bidirectional lncRNAs (the coding transcript is initiated in a genomic region of less than 1,000 bp).

FIGURE 2

Traumatic brain injury (TBI)-related long non-coding RNA (lncRNA) regulatory mechanisms and pathways. Different types of lncRNAs regulate various downstream molecules that exert neuroprotective or neuroapoptotic effects by inducing cell death pathways, such as inflammatory pathways, oxidative stress, autophagy, and ferroptosis.

FIGURE 3

Long non-coding RNA (lncRNA) molecular pattern diagram in traumatic brain injury (TBI). In traumatic brain injury, the expression of lncRNA downstream molecules increases, which activates the inflammation pathway. At the same time, the permeability of the blood-brain barrier increase, thereby releasing inflammatory factors. Both factors will affect secondary brain injury.