Rapamycin and senescence in irradiated human coronary endothelial cells
In cultured human coronary artery endothelial cells, ionising radiation produced senescence features and signs of early pro-atherogenic dysfunction; rapamycin attenuated these effects. This is in vitro work, not evidence of benefit in people. [1]
Automatic summary · not editorially reviewed
The key findings
In cultured human coronary artery endothelial cells, ionising radiation induced cellular senescence and a pro-atherogenic phenotype, and rapamycin attenuated these effects. [1]
Irradiated cells showed elevated senescence-associated-β-galactosidase activity, nuclear enlargement, increased Cyclin dependent kinase inhibitor 1 A and p53 expression, impaired barrier integrity and heightened monocyte adhesion. [1]
The authors describe senescence as a driver of pro-atherogenic phenotypes in HCAECs in vitro and call mTOR inhibition a promising strategy against radiation-associated endothelial dysfunction. [1]
The source at a glance
- Study type / format
- In vitro laboratory study (abstract)
- Population / context
- Human coronary artery endothelial cells (HCAECs) studied in vitro
- Summary based on
- Study abstract
- Original publication
- June 30, 2026
Irradiated coronary endothelial cells in culture
The abstract describes experiments in human coronary artery endothelial cells (HCAECs) grown in the laboratory. Ionising radiation is named as a recognised risk factor for cardiovascular disease, but the mechanisms linking exposure to it remain incompletely understood. The authors report that radiation drove a pro-atherogenic phenotype in these cells through induction of cellular senescence, and that rapamycin attenuated these effects.
Supporting source [1]
Senescence markers and impaired barrier function
Irradiated cells showed hallmark senescence features: elevated senescence-associated-β-galactosidase activity, nuclear enlargement, and increased expression of Cyclin dependent kinase inhibitor 1 A and p53. Functionally, irradiated HCAECs displayed impaired barrier integrity and heightened monocyte adhesion. Profiling of gene and protein expression revealed broad radiation-induced changes enriched in DNA damage response, cell-cycle arrest, senescence, proteostasis and immune-related pathways.
Supporting source [1]
In vitro scope and proposed mTOR strategy
The authors conclude that senescence is a driver of pro-atherogenic phenotypes in HCAECs in vitro and identify mTOR inhibition as a promising strategy against radiation-associated endothelial dysfunction. They position senescence as a tractable therapeutic target in radiation-induced vascular injury. These are laboratory findings in one cell type; the abstract reports no human participants, clinical outcomes or long-term follow-up, so they do not show that rapamycin prevents cardiovascular disease in people.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. Findings come from human coronary artery endothelial cells in culture, with no human participants, clinical outcomes or follow-up reported. The abstract does not establish that rapamycin prevents cardiovascular disease in people.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Whiteman C. · europepmc.org · June 30, 2026