Structured evidence table for Pterostilbene Menopause Transition Trial, generated from 1 reusable source document in the Migaku knowledge base.
| topic | claim | evidence level | citation | source |
|---|---|---|---|---|
| Pterostilbene Menopause Transition Trial | However, accumulating evidence over the past decade has revealed that these processes are tightly interconnected within a complex regulatory network. | 3 | Bahar Md Entaz (2026) | The autophagy-senescence axis as a threshold model of aging and therapeutic targeting |
| Pterostilbene Menopause Transition Trial | Although autophagy suppresses senescence initiation, growing evidence indicates that it is also required for the maintenance and persistence of established senescent cells []. | 3 | Bahar Md Entaz (2026) | The autophagy-senescence axis as a threshold model of aging and therapeutic targeting |
| Pterostilbene Menopause Transition Trial | Senescent cells remain metabolically active and adopt a hypersecretory state characterized by the senescence-associated secretory phenotype (SASP), which includes pro-inflammatory cytokines, growth factors, and proteases that disrupt tissue homeostasis [,]. | 3 | Bahar Md Entaz (2026) | The autophagy-senescence axis as a threshold model of aging and therapeutic targeting |
| Pterostilbene Menopause Transition Trial | 1 2 3 4 5 Macroautophagy and cellular senescence are evolutionarily conserved stress-response programs that play essential roles in maintaining cellular homeostasis and tissue integrity []. | 3 | Bahar Md Entaz (2026) | The autophagy-senescence axis as a threshold model of aging and therapeutic targeting |
Source documents