The Role Of Tom40 In Dental Pulp Fibroblasts Under Pulpitis

To investigate the mechanism by which TOM40, a subunit of the mitochondrial outer membrane translocase (TOM) complex, regulates mitochondrial respiratory function in human dental pulp fibroblasts (hDPFs) under inflammatory conditions. A rat molar pulpitis model was established via pulp exposure to evaluate inflammatory infiltration and identify TOM complex subunits with altered expression via transcriptome sequencing. In vitro, hDPFs were stimulated with lipopolysaccharide (LPS) to assess mitochondrial respiratory function and respiratory chain protein transport. TOM40-knockdown and TOM40-overexpressing hDPF cell lines were constructed to further examine TOM40′s regulatory effects. In the pulpitis model, TOM40 expression was specifically downregulated. LPS stimulation or TOM40 knockdown disrupted respiratory chain protein transport and impaired mitochondrial respiration in hDPFs. Conversely, TOM40 overexpression restored protein transport and rescued mitochondrial respiratory function. Under inflammatory stress, TOM40 downregulation disrupts respiratory chain protein transport in hDPFs, leading to mitochondrial respiratory dysfunction. Targeting TOM40 may mitigate inflammation-induced mitochondrial impairment in dental pulp.