Researchers from leading longevity institutes highlight senolytics that selectively eliminate senescent cells via Bcl-2 family inhibition, reducing SASP-driven inflammation in mouse studies while epigenetic reprogramming via transient Yamanaka factor activation restores youthful gene expression, together offering promising routes to extend healthspan.
Key points
- Senolytics targeting Bcl-2 family proteins ablate senescent cells in aged mice, decreasing SASP factors by over 50% and improving tissue function.
- Transient OSKM factor expression reprograms aged fibroblasts, reversing DNA methylation age and restoring proteostasis in vitro.
- Fasting-mimicking diets activate autophagy and reduce IGF-1 signaling in rodent models, delivering caloric restriction benefits without chronic hunger.
Why it matters: These advances shift longevity research from symptom management to fundamental reversal of aging mechanisms, offering targeted interventions for healthspan extension.
Q&A
- What are senolytics?
- How does cellular reprogramming reverse aging?
- What is the Hallmarks of Aging framework?
- Why use fasting-mimicking diets instead of calorie restriction?