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gingivalis infection in periodontitis upregulates NCOA4 via the NF-κB pathway, promoting ferritin lysosomal degradation and causing a continuous influx of ferrous iron (Fe 2+ ) into the labile iron pool (LIP) ( 2.1.2 Impaired iron efflux and pathological iron accumulation Recurrent microbleeding within the periodontal pocket is a core feature distinguishing periodontitis from other chronic inflammatory diseases and represents the most direct source of iron overload

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In support of this hypothesis, six of these DEGs ( TNXRD1 , SRXN1, GCLM, AKR1B10, OSGIN1, and TRIM16L) are already known to be direct NRF2 transcriptional targets [41,42,43,44,45,46]