Fight Aging! Newsletter, March 1st 2021

This study may have important implications for preventing cell senescence and aging-induced tendinopathy, as well as for the selection of novel therapeutic targets of chronic tendon diseases.

Our results showed that the treatment of bleomycin, a DNA damaging agent, induced rat patellar TSC (PTSC) cellular senescence. The senescence was characterized by an increase in the senescence-associated β-galactosidase activity, as well as senescence-associated changes in cell morphology. On the other hand, rapamycin could extend lifespan in multiple species, including yeast, fruit flies, and mice, by decelerating DNA damage accumulation and cellular senescence. As an inhibitor of mTOR, rapamycin is a prospect of pharmacological rejuvenation of aging stem cells. Our findings show that rapamycin partially decreases the senescence-associated β-gal activity and morphological alterations, which indicate that rapamycin reverses senescence in rat PTSCs at both molecular and cellular levels.

Autophagy is a major mechanism for maintaining cellular homeostasis via autophagic cell death. Studies have shown that the activity of autophagy is constitutively high in mesenchymal, hematopoietic, dermal, and epidermal stem cells. Autophagy plays a key role in the control of self-renewal and the stemness of stem cells, and growing evidences have linked autophagy and the mTOR signaling pathway. Some proposed underlying antiaging mechanisms by rapamycin include downregulated translation, in...

Source: Fight Aging! - February 28, 2021 Category: Research Authors: Reason Tags: Newsletters Source Type: blogs