Study on the Correlation Between NF-κB and Central Fatigue

Abstract

In recent years, the World Health Organization (WHO) has included fatigue as a major risk factor for human life and health. The incidence rate of fatigue is high. In Europe and America, nearly 1/3 of the population is suffering from fatigue. Due to the acceleration of modern people’s life rhythm and the increase of work pressure, more and more attention has been paid to central fatigue. The activation of NF-κB is related to central fatigue, which has been paid little attention by previous studies. At the same time, previous studies have mostly focused on the immune regulation function of NF-κB, while the NF-κB pathway plays an equally important role in regulating nerve function. NF-κB can participate in the occurrence and development of central fatigue by mediating immune inflammatory response, regulating central excitability and inhibitory transmitters, regulating synaptic plasticity and regulating central nervous system (CNS) functional genes. In addition to neuroprotective effects, NF-κB also has nerve damage effects, which is also closely related to the occurrence and development of central fatigue. In this review, we focus on the relationship between NF-κB pathway and central fatigue and further explore the biological mechanism of central fatigue. At the same time, the clinical application and potential of typical NF-κB inhibitors in the treatment of fatigue were analyzed to provide reference for the clinical treatment of central fatigue.

Aberrations in the Cross-Talks Among Redox, Nuclear Factor-κB, and Wnt/β-Catenin Pathway Signaling Underpin Myalgic Encephalomyelitis and Chronic Fatigue Syndrome

“…All in all, the results of our network and enrichment analysis and Maes et al (35,36) indicate that the complex cross-talks between NF-κB and ROS signaling are involved in the pathophysiology of CFAS-D. Moreover, recent studies show that increased NF-κB expression may be associated with central fatigue by modulating central nervous system genes and regulating immune-inflammatory processes, synaptic plasticity, and memory and exerting neurotoxic effects (35)(36)(37).…”

Fatigue, Toll-Like Receptor 4, and Pro-Inflammatory Cytokines in Adults With Subarachnoid Hemorrhage: A 6-Month Longitudinal Study

“…The effects of NF-kappa B activation on neuronal damage and released cytokines are important mechanisms in central fatigue (Yang et al, 2021). Central fatigue results from disrupted changes or the central nervous system's normal activation process (Yang et al, 2021). In SAH survivors, the dopamine imbalance hypothesis was suggested as one of the mechanisms contributing fatigue (Western et al, 2020).…”

“…Expression of TLR4 on day 1 post-SAH has also been associated with poor functional outcomes at 3 months post-SAH (Ma et al, 2015b). The effects of NF-kappa B activation on neuronal damage and released cytokines are important mechanisms in central fatigue (Yang et al, 2021). Central fatigue results from disrupted changes or the central nervous system’s normal activation process (Yang et al, 2021).…”

Broken Connections: The Evidence for Neuroglial Failure in ME/CFS

“…379 Physiologically, both the stress response and the immune response seem to be intricately linked because the stress response is based on intense crosstalk with the transcription factor Nuclear Factor-kappa B (NF-κB), a potent activator of the innate immune response and implied by several groups in the pathology of ME/CFS 380,381 and indeed closely related to fatigue symptomatology. 382 Inflammatory processes and the stress response are also linked on other functional levels (and, as frequently observed, cerebral blood flow functions may be included in this link). High lactate levels, for example, e.g.…”