The Potential Role of m(6)A in the Regulation of TBI-Induced BGA Dysfunction

The brain–gut axis (BGA) is an important bidirectional communication pathway for the development, progress and interaction of many diseases between the brain and gut, but the mechanisms remain unclear, especially the post-transcriptional regulation of BGA after traumatic brain injury (TBI). RNA methylation is one of the most important modifications in post-transcriptional regulation. N6-methyladenosine (m(6)A), as the most abundant post-transcriptional modification of mRNA in eukaryotes, has recently been identified and characterized in both the brain and gut. The purpose of this review is to describe the pathophysiological changes in BGA after TBI, and then investigate the post-transcriptional bidirectional regulation mechanisms of TBI-induced BGA dysfunction. Here, we mainly focus on the characteristics of m(6)A RNA methylation in the post-TBI BGA, highlight the possible regulatory mechanisms of m(6)A modification in TBI-induced BGA dysfunction, and finally discuss the outcome of considering m(6)A as a therapeutic target to improve the recovery of the brain and gut dysfunction caused by TBI.