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Comment
. 2023 Aug;33(8):575-576.
doi: 10.1038/s41422-023-00842-y.

Senolysis through thrombomodulation

Corey M Webster  1 , Jan M van Deursen  2
Affiliations
Comment

Senolysis through thrombomodulation

Corey M Webster et al. Cell Res. 2023 Aug.
No abstract available

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Figures

Fig. 1
Fig. 1. THBD joins a subset of immediate-early stress response factors that promote the formation and survival of SNCs.
Most cellular stresses activate p53, which in turn induces various pro-apoptotic target genes as well as p21, which dramatically alters the transcriptome through hypophosphorylation of the Rb transcription factor, resulting in rapid cell cycle arrest and concomitant generation of the PASP. The PASP includes RNASE4 and THBD, which together with two other immediate-early stress response proteins, ANG and BCL-xL, mount a prosurvival response that counteracts apoptosis and steer cells beyond repair to the alternative cell fate of cellular senescence. Once senescent, cells continue to depend on each of these immediate-early survival factors, as illustrated by the observation that their depletion causes SNC death. Small-molecule senolytics have been identified that target BCL-xL or THBD for inhibition.
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