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3.4. Nrf2 and Inflammation From International Journal of Medicine

Inflammatory pathways protect from exogenous harmful stimuli and, to some extent, from intrinsic dysregulation of cell proliferation that may lead to neoplastic growth. However, inflammation may also take place during aberrant self-reactivity in autoimmune diseases [127], while a low but chronic level of inflammation in the absence of real exogenous or endogenous threats is a common hallmark of aging (inflammaging) and aging-related diseases [128,129]. Nrf2 is able to modulate inflammation through multiple mechanisms, such as the regulation of redox homeostasis and the suppression of pro-inflammatory genes, either directly or through the interaction with NF-κB. Inflammation increases local and systemic ROS level while ROS enhance inflammation [130]. The Nrf2-mediated ROS-homeostatic control is able to break this vicious cycle. Nrf2 reduces inflammation by preventing the recruitment of RNA polymerase II to start gene transcription of pro-inflammatory cytokines IL-6 and IL1β [131]. In addition, Nrf2 tunes gene expression in inflammatory macrophages through a bidirectional crosstalk with NF-κB transcription factor, and regulates the transcription of Nrf2 itself [132] that, in turn, inhibits the transcriptional activity of NF-κB [133]. NF-κB has long been recognized as a point of convergence of inflammation and aging, and the array of NF-κB-regulated genes largely overlaps with the targets of transcriptional/epigenetic regulators such as sirtuins that have been demonstrated to promote lifespan extension [134,135,136]. This notion once again corroborates the ontological link between inflammation and aging and allows speculation that O3-induced activation of Nrf2 might be a potential tool to prevent aging and prolong lifespan.

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