Research
Hormonal
Inhibition of mTORC1 by rapamycin extends lifespan in multiple species by enhancing autophagy and mitophagy, thereby maintaining mitochondrial homeostasis.
Rapamycin extends lifespan in model organisms by boosting cellular cleanup (autophagy/mitophagy). While effective, chronic use has side effects. Dietary restriction also activates this pathway, offering a natural way to achieve similar benefits without pharmaceutical intervention.
GoodSupportsHIGH confidence
Rapamycin has been consistently shown to prolong lifespan in various species ranging from worm to mouse... Key mechanisms for the increased longevity effects of mTORC1 inhibition are thought to include... enhanced autophagy flux
Why this rating
Consistent lifespan extension in yeast, worms, flies, and mice.
Source
Mitochondria in the signaling pathways that control longevity and health span
Mansour Akbari et al. · Ageing Research Reviews · 2019
DOI 10.1016/j.arr.2019.100940
narrative_reviewCited 207×
Read the paper DOI resolved against Crossref · corpus check 2026-06-10
More from this paper
- Inhibition of the Insulin/IGF-1 Signaling (IIS) pathway extends lifespan in multiple species by enhancing mitochondrial function, biogenesis, and mitophagy.Good
- Activation of AMPK by dietary restriction or compounds like metformin extends lifespan by inhibiting mTOR and promoting mitochondrial biogenesis.Good
- Mild mitochondrial stress and modest increases in mitochondrial ROS levels increase lifespan in C. elegans, demonstrating that ROS acts as a beneficial signaling molecule rather than solely as a damaging agent.Moderate
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