Full text is available at the source.
Abstract
Short-term inhibition of CDK4/6 with abemaciclib reduces systemic NASP expression and improves physical function in mice following chemotherapy.
- Senescent cells accumulate and contribute to dysfunction through a pro-inflammatory process associated with aging and chemotherapy.
- Abemaciclib was shown to suppress established NF-κB-associated senescence in both laboratory and living mouse models.
- Inhibition of CDK4/6 diminished the pro-tumorigenic activity of chemotherapy-induced senescent cells.
- Genetic knockdown of CDK4/6 produced effects similar to those seen with abemaciclib, indicating a dependency on this pathway.
- CDK4/6 inhibition interfered with retinoic acid signaling, affecting NASP expression.
- Interactions between CDK4/6 and NF-κB were disrupted by abemaciclib, suggesting a potential therapeutic target for reducing the impact of senescent cells.
Simplified
Longevity & Aging