A chemical signal lowers energy output in blood vessel muscle cells
In experiments with blood vessel muscle cells, the signal also promoted an inflammatory state and impaired mitochondria, the cells’ energy-producing structures.
Edited by Boris Djordjevic · AgingResearch.News
Researchers studied C57BL/6J mice aged 2 to 22 months and vascular smooth muscle cells, the muscle cells in blood vessel walls, in animal and cell experiments. They used chemicals to induce senescence, a state in which cells stop dividing, in the cell models.
Levels of prostaglandin E2, a signaling molecule, and EP2, its receptor, were higher in aging mouse aortas and senescent cells. In cell experiments, activating this signaling pathway pushed cells toward an inflammatory state and impaired mitochondrial function. It reduced production of ATP, a molecule that carries usable energy. The pathway also increased QSOX1, a downstream protein. Blocking EP2 or reducing QSOX1 improved mitochondrial function and reduced senescence markers. Researchers also mapped the structure of EP2 bound to an inhibitor to support future drug screening.
Why it matters
Blood vessel aging contributes to age-related chronic diseases. The work points to a possible molecular target for research on slowing these vessel changes.
Caveats
The cell experiments did not establish whether targeting this pathway delays blood vessel aging or reduces cardiovascular risk in people. This conference abstract reported no sample sizes.
The paper
Tongji Hospital- Tongji Medical College
ESC Congress 2026 Abstract, Oct 26, 2026
Presented at ESC Congress 2026
