Senescent human cardiac cells and fibrin clot formation in the laboratory
In laboratory experiments, doxorubicin-induced senescence of human cardiac fibroblasts and cardiac endothelial cells accelerated fibrinogen polymerization, increased thrombin generation and impaired fibrinolysis; rapamycin attenuated the polymerization. These are cell-culture findings, not evidence of human lifespan or treatment benefit. [1]
Automatic summary · not editorially reviewed
The key findings
In doxorubicin-induced senescence of human cardiac fibroblasts and cardiac endothelial cells, senescence accelerated and amplified fibrinogen polymerization. [1]
Senescent cells impaired thrombus resolution by suppressing plasminogen activation and downstream fibrinolysis. [1]
Senescence-mediated fibrinogen polymerization was dose dependent and attenuated by the senostatic agent rapamycin. [1]
The source at a glance
- Study type / format
- Laboratory cell study (abstract)
- Population / context
- Human cardiac fibroblasts and cardiac endothelial cells made senescent with doxorubicin in laboratory experiments.
- Summary based on
- Study abstract
- Original publication
- August 1, 2026
Senescent cardiac cells and fibrinogen polymerization
The abstract notes that thrombosis risk rises markedly with age, but the cellular mechanisms linking aging and clot formation remain incompletely understood. The authors examined doxorubicin-induced senescence in human cardiac fibroblasts and cardiac endothelial cells. In both cell types, senescence accelerated and amplified fibrinogen polymerization, the process in which soluble fibrinogen is converted into fibrin monomers that form the clot mesh.
Supporting source [1]
Thrombin mediation and impaired fibrinolysis in senescent cells
A thrombin inhibitor reduced the polymerization and the cleavage of a thrombin-specific substrate by senescent cells, implicating thrombin as a key mediator. Senescent cells also impaired thrombus resolution by suppressing plasminogen activation and downstream fibrinolysis. Gene expression analysis showed senescence-associated upregulation of procoagulant and antifibrinolytic mediators, consistent with the functional effects.
Supporting source [1]
Dose dependence and rapamycin effect in this cell model
The abstract reports that senescence-mediated fibrinogen polymerization was dose dependent and attenuated by the senostatic agent rapamycin. The authors describe these findings as a direct mechanistic link between cellular senescence and thrombosis in cardiac cells and highlight senescence as a potential therapeutic target in age-related thrombotic disease. This is a proposed mechanism from cell experiments; it does not show that rapamycin prevents or treats thrombosis in people.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. All results come from laboratory experiments on human cardiac fibroblasts and endothelial cells made senescent with doxorubicin. The abstract reports no human participants, clinical outcomes or lifespan data, so the proposed link to age-related thrombotic disease and the therapeutic targeting of senescence remain untested here.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Shahar T, Ezra N, Chen S, Kryukov O, Cohen S. · europepmc.org · August 1, 2026