EIF2AK3 and pulpitis: This study elucidates the PERK-centred regulatory mechanism in MAMs that governs inflammation-impaired odontogenic differentiation of hDPSCs, potentially involving IP3R-dependent calcium flux and dynamic protein interactions in MAMs.<h4>Methods</h4>Rat pulpitis models and in vitro lipopolysaccharide (LPS)-induced inflammatory models of hDPSCs were established to investigate the effects of PERK signalling in odontogenesis under inflammatory conditions.