Peptidylarginine deiminase in Porphyromonas gingivalis-derived outer membrane vesicles exacerbates metabolic dysfunction-associated steatotic liver disease through the NPAS2/CYP4A10 pathway

strains, from which OMVs were isolated. The results of the in vivo and in vitro experiments indicated that PPAD-enriched OMVs mediated hepatic metabolic dysregulation via suppression of the circadian regulator NPAS2 and downstream inhibition of CYP4A10 expression, revealing a previously unrecognized PPAD-liver communication pathway. These findings highlight the urgent need for effective PPAD inhibitors and a deeper understanding of the interactions of PPAD with host proteins implicated in systemic diseases, underscoring the broader health impacts of periodontal disease.