Selenoprotein P attenuates oxidative senescence and ferroptosis-associated lipid peroxidation in dental pulp stem cells through a FOXM1-dependent program

Figure 1 Integrated single-cell RNA-sequencing analysis reveals erosion of the selenium-dependent antioxidant program in aged dental pulp mesenchymal stem cell populations. A: Uniform manifold approximation and projection plot showing integrated clustering of cells from young and aged human dental pulp tissues; major cell populations are annotated based on canonical markers; B: Uniform manifold approximation and projection split by age group (young vs aging), showing age-related changes in cell distribution across clusters; C: Quantitative cell composition analysis showing the relative proportion of major cell populations, including contraction of the dental pulp stem cell/mesenchymal stem cell compartment in aged pulp; D: Gene Ontology enrichment analysis of downregulated genes in the mesenchymal lineage from aged pulp, highlighting redox-related biological processes; E: Pathway enrichment summary showing suppression of selenium metabolism/glutathione-related pathways in aged mesenchymal cells; F: Heatmap or dot plot showing reduced expression of selenium transport and selenium-dependent antioxidant genes in aged mesenchymal cells, including selenoprotein P, glutathione peroxidase 1/4, thioredoxin reductase 1/3, and DIO2/3. Data are presented as mean ± SD. UMAP: Uniform manifold approximation and projection; DPSCs: Dental pulp stem cells; ECs: Endothelial cells; ScCs: Schwann cells; nmScCs: Nonmyelinating Schwann cells; DEGs: Differentially expressed genes; MSC: Mesenchymal stem cell; GPx: Glutathione peroxidase; TXNRD: Thioredoxin reductase; SELENOP: Selenoprotein P.