For those who were intrigued by yesterday’s post about the reversal of dermal aging by blockade of NF-κB, I wanted to point our a few more interesting tidbits related to everyone’s favorite inflammatory transcription factor.
- Skin is not the only organ in which aging can be reversed by attacking NF-κB activity. In the immune system, Huang et al. report that pharmaceutical inhibition of NF-κB blocks age-related increases in inflammatory cytokine production. The study focuses on a class of helper T cells that have been implicated in both immune senescence and autoimmune pathologies.
- Mourkioti and Rosenthal review the role of NF-κB in muscle, and discuss several mechanisms by which the factor might influence age-related muscle disease.
- Finally, Li et al. demonstrate that the MULAN protein is a mitochondrial ubiquitin E3 ligase that regulates mitochondrial dynamics. Prior work had shown MULAN to be an activator of NF-κB, so this study may be the first step toward establishing a novel signaling pathway between the mitochondria and the nucleus. (Brainstorming topic: Under what conditions would the mitochondria want to instruct the nucleus to produce inflammatory cytokines?). Their paper is at PLoS ONE, so reader comments are welcomed.