[DOI] [PubMed] [Google Scholar] 49.Lou H, Kaplowitz N: Glutathione Depletion Down-regulates Tumor Necrosis Factor -induced NF-B Activity via IB Kinase-dependent and -independent Mechanisms
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This section moves beyond a deterministic view of SFN bioavailability to focus on the host factorsspecifically the gut microbiome and host geneticsthat act as key determinants of efficacy
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Atherosclerosis progression, as a chronic inflammatory mechanism, is characterized by immune system dysregulation associated with increased pro-inflammatory cytokine production, including interleukin 6 (IL-6), tumor necrosis factor- (TNF-), and IL-1, as well as pattern recognition receptor proteins like CRP (170, 261267)
