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.

The Role of Microglial Exosomes and miR-124-3p in Neuroinflammation and Neuronal Repair after Traumatic Brain Injury

“…Moreover, miR-124-3p might not be the only microRNA contained by the microglial exosomes that could exert beneficial effects in TBI, not only within the brain cells but also in other affected tissues. Thus, further studies could focus on describing the microRNA content of microglial exosomes and specifically studying their effects on brain and bone tissues, as also seen for miR-21-5p [ 78 , 79 ] or miR-195, which targets NOD-like receptor X1 that interacts with the NF-κB signaling pathway by inhibiting it and preventing the inflammatory response during secondary brain injury and thus promoting structural and functional recovery after TBI [ 80 ].…”

Inflammatory response in traumatic brain and spinal cord injury: The role of XCL1‐XCR1 axis and T cells

“…The pathophysiological mechanisms that underlie secondary injury comprise a range of processes, including glutamate excitotoxicity, mitochondrial dysfunction, oxidative stress, lipid peroxidation, neuroinflammation, axonal degeneration, and apoptotic cell death 8,29,32,36,37 . Of these processes, the inflammatory response significantly impacts secondary damage.…”

“…8,35 The pathophysiological mechanisms that underlie secondary injury comprise a range of processes, including glutamate excitotoxicity, mitochondrial dysfunction, oxidative stress, lipid peroxidation, neuroinflammation, axonal degeneration, and apoptotic cell death. 8,29,32,36,37 Of these processes, the inflammatory response significantly impacts secondary damage. The inflammatory response of the CNS is an aseptic inflammatory response characterized by the overproduction of various cytokines and chemokines and the massive accumulation of different immune cells in the inflammatory area.…”