(IMAGE)
Caption
Inflammation and mitochondrial function as mechanisms in accelerated aging (AA) across substance use disorders (SUDs). This figure presents a proposed model linking genes associated with neuroinflammatory and oxidative stress-related pathways across three major SUDs when comparing accelerated aging positive (AA+) and accelerated aging negative (AA−). Genes that are shown in yellow were observed in aging-related pathways within AUD, while the ones in green were observed in aging-related pathways within StUD, and the ones in blue within OUD. The nuclear factor-kappa B (NF-κB) pathway is activated by genes such as NR4A3, TRIM21, IFITM2, IFITM3, and IL-32, which are involved in inflammatory signaling and immune regulation and might contribute to the production of proinflammatory cytokines (e.g., IFN-α, IFN-γ , TNF-α, IL-6) that may exacerbate neuronal damage. Furthermore, the TXNIP and HDAC1 contribute to inflammasome activation, leading to
increased Caspase-1 activity and the subsequent maturation of IL-1β and IL-18, promoting neuroinflammatory responses. Future studies might investigate the role of NLRP3 as a central component in stimulant-induced neuroinflammation in this mechanism. Finally, the upregulation of NOS3, TXNIP, CSF1, HTR2A, HDAC1, EDN1, THBS1, and RELN is linked to vascular dysfunction, cellular stress, and neurodegeneration, might contribute to mitochondrial dysfunction and oxidative
stress (ROS).
Credit
Consuelo Walss-Bass
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