| First Author | Sun S | Year | 2023 |
| Journal | Nat Aging | Volume | 3 |
| Issue | 11 | Pages | 1401-1414 |
| PubMed ID | 37946040 | Mgi Jnum | J:361269 |
| Mgi Id | MGI:7857079 | Doi | 10.1038/s43587-023-00512-z |
| Citation | Sun S, et al. (2023) CD133(+) endothelial-like stem cells restore neovascularization and promote longevity in progeroid and naturally aged mice. Nat Aging 3(11):1401-1414 |
| abstractText | The stem cell theory of aging dictates that a decline in the number and/or function of stem cells causes tissue degeneration and aging; however, it still lacks unequivocal experimental support. Here, using lineage tracing and single-cell transcriptomics, we identify a population of CD133(+) bone marrow-derived endothelial-like cells (ELCs) as potential endothelial progenitor cells, which contribute to tubular structures in vitro and neovascularization in vivo. We demonstrate that supplementation with wild-type and young ELCs respectively restores neovascularization and extends lifespan in progeric and naturally aged mice. Mechanistically, we identify an upregulation of farnesyl diphosphate synthase (FDPS) in aged CD133(+) ELCs-a key enzyme in isoprenoid biosynthesis. Overexpression of FDPS compromises the neovascularization capacity of CD133(+) ELCs, whereas FDPS inhibition by pamidronate enhances neovascularization, improves health measures and extends lifespan in aged mice. These findings highlight stem cell-based strategies for the treatment of progeria and age-related pathologies. |
