Metabolic protein limited blood vessel growth in engineered mice
Deleting the protein’s gene reversed impaired vessel growth in mice engineered to have blood vessel lining cells that had stopped dividing.
Limit: Compound benefits came from cells, not treated animals
Edited by Boris Djordjevic · AgingResearch.News
Experiments in blood vessel lining cells and genetically engineered mice tested how senescence, a state in which cells stop dividing, affected blood vessel growth. Senescent cells had more TIGAR, a protein that limits sugar breakdown for energy. They had less capacity to break down sugar and were worse at moving and forming tube-like structures than young cells.
Silencing the TIGAR gene restored sugar breakdown capacity and improved these functions in senescent cells. Mice engineered to have senescent blood vessel lining cells recovered blood flow less well than unmodified mice after researchers restricted blood supply to a hindlimb. Deleting TIGAR completely reversed impaired blood vessel growth in these mice. The researchers also identified a compound that restored movement and vessel-forming functions in senescent cells.
Why it matters
Diseases that restrict blood supply are a concern in aging. The findings suggest a possible treatment strategy focused on how senescent blood vessel lining cells use energy.
Caveats
The compound’s reported benefits came from cells, not treated animals; testing in aged mice was ongoing. This conference abstract reported neither sample sizes nor tests in people.
The paper
Senescence-associated metabolic shift impedes endothelial angiogenic functions
Kyoto Prefectural University of Medicine
ESC Congress 2026 Abstract, Oct 26, 2026
Presented at ESC Congress 2026
