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A landmark study by Regland et al

doi: 10.1016/s0024-3205(00)00803-1

Their functional enrichment analyses linked these genes to mRNA metabolic processes, immune cell regulation, and RNA transport pathways, confirming their potential role in OA pathogenesis and immune-mediated joint degradation (Huo et al., 2025)

It is then tempting to speculate that in those critically ill patients with the worst outcomes (death or chronicity) an early pro-inflammatory stage could result in decreases in cellular NAD + and a subsequent failure of SIRT3 to prevent LCAD and glycolytic enzyme hyperacetylationthis would not only result in impaired fatty acid oxidation and subsequent cellular lipid accumulation, but also the acetylation of numerous mitochondrial proteins and glycolytic enzymes with subsequent immunoparesis and chronic organ dysfunction, as seen in sepsis and CKD (177, 190, 193, 253, 263)