A recent study reveals that imbalanced nucleotide metabolism triggers inflammation via mitochondrial DNA (mtDNA) instability. Researchers found that ribonucleotides, when incorrectly incorporated into mtDNA, lead to its instability and subsequent release into the cytosol, activating the cGAS-STING immune signaling pathway. Investigation in mice lacking the MGME1 exonuclease showed a link between ribonucleotide levels and age-related renal inflammation. Additionally, cellular senescence contributed to mtDNA leakage, suggesting metabolic strategies that could mitigate age-associated inflammatory processes.
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