Antagonistic crosstalk between NF-κB and SIRT1 in the regulation of inflammation and metabolic disorders.
Level 5 - mechanism / opinion, no new human data
Narrative review describing molecular mechanisms without systematic search methodology or new empirical human data
PubMed 23770291 · doi:10.1016/j.cellsig.2013.06.007
What was done
Narrative review of published literature examining the molecular mechanisms of antagonistic crosstalk between NF-κB and SIRT1 signaling pathways in the regulation of inflammation and energy metabolism.
What was found
The abstract reports no quantitative values or statistical findings. It describes mechanistic pathways: SIRT1 suppresses NF-κB signaling directly through p65 subunit deacetylation and indirectly via AMPK, PPARα, and PGC-1α activation, promoting oxidative metabolism. Conversely, NF-κB down-regulates SIRT1 activity via miR-34a, IFNγ, and reactive oxygen species, driving glycolytic flux and chronic inflammatory signaling.
Why it matters
It summarizes a key molecular axis linking metabolic dysfunction to chronic inflammation, helping conceptualize potential shared targets for metabolic and age-related inflammatory diseases.
Limits
Narrative review design without systematic search criteria, meta-analytic pooling, effect sizes, or primary human empirical data. All claims are mechanistic summaries.
Cited by
- supports NF-kappa-B-mediated pro-inflammatory signaling and SIRT1-mediated anti-inflammatory pathways exhibit mutual inhibition.