OTULIN Can Improve Spinal Cord Injury by the NF-κB and Wnt/β-Catenin Signaling Pathways.
Qianhui WangLvxia WangBenson O A BotchwayYong ZhangMin HuangXuehong LiuPublished in: Molecular neurobiology (2024)
Spinal cord injury (SCI) is a significant health concern, as it presently has no effective treatment in the clinical setting. Inflammation is a key player in the pathophysiological process of SCI, with a number of studies evidencing that the inhibition of the NF-κB signaling pathway may impede the inflammatory response and improve SCI. OTULIN, as a de-ubiquitination enzyme, the most notable is its anti-inflammatory effect. OTULIN can inhibit the NF-κB signaling pathway to suppress the inflammatory reaction via de-ubiquitination. In addition, OTULIN may promote vascular regeneration through the Wnt/β-catenin pathway in the wake of SCI. In this review, we analyze the structure and physiological function of OTULIN, along with both NF-κB and Wnt/β-catenin signaling pathways. Furthermore, we examine the significant role of OTULIN in SCI through its impairment of the NF-κB signaling pathway, which could open the possibility of it being a novel interventional target for the condition.
Keyphrases
- signaling pathway
- spinal cord injury
- pi k akt
- spinal cord
- epithelial mesenchymal transition
- cell proliferation
- induced apoptosis
- stem cells
- inflammatory response
- neuropathic pain
- oxidative stress
- lps induced
- healthcare
- minimally invasive
- mental health
- immune response
- health information
- social media
- combination therapy
- nuclear factor
- endoplasmic reticulum stress