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Senolytic therapy increases replicative capacity by eliminating senescent endothelial cells.

Hossein Abdeahad1, Denisse G Moreno2, Samuel I Bloom3

  • 1Department of Nutrition and Integrative Physiology, University of Utah, Salt Lake City, UT, USA.

Experimental Gerontology
|September 10, 2025
PubMed
Summary

Senolytics like Talabostat and Navitoclax clear senescent endothelial cells, promoting proliferation in aged cultures. Talabostat shows greater efficacy by reducing oxidative stress and improving genomic integrity in these aging cells.

Keywords:
Endothelial senescenceMitochondrial ROSSenolyticsTelomere dysfunctionVascular aging

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Area of Science:

  • Gerontology
  • Cardiovascular Biology
  • Cellular Biology

Background:

  • Aging is a primary risk factor for cardiovascular diseases (CVD), marked by inflammation, oxidative stress, and cellular senescence.
  • Senescent endothelial cells (ECs) contribute to vascular dysfunction and CVD progression.
  • Senolytics eliminate senescent cells, but their impact on aged endothelial cell function is not fully understood.

Purpose of the Study:

  • To investigate the effects of senolytics Talabostat and Navitoclax on aged endothelial cell cultures.
  • To assess the impact of senolytic treatment on endothelial cell proliferation, senescence markers, DNA damage, and telomere dysfunction.

Main Methods:

  • Replicative senescent human umbilical vein endothelial cells (HUVECs) were treated with Talabostat (10 μM) or Navitoclax (1.0 μM).
  • Evaluated senescent cell burden, cumulative population doublings, telomere length, DNA damage markers (53BP1), telomere dysfunction-induced foci (TIFs), and mitochondrial reactive oxygen species (mtROS).

Main Results:

  • Both Talabostat and Navitoclax reduced senescent cell burden and increased endothelial cell proliferation.
  • Talabostat treatment decreased telomere length, 53BP1, and TIFs, suggesting replication-associated telomere attrition.
  • Navitoclax increased mtROS and did not improve DNA damage or telomere dysfunction markers.

Conclusions:

  • Both senolytics reduce senescent endothelial cell burden and enhance proliferation in aged cultures.
  • Talabostat demonstrates superior efficacy, associated with reduced oxidative stress and improved genomic integrity.
  • Findings highlight differential effects of senolytics on aging endothelial cells, offering insights for CVD therapeutic strategies.