Skip to content
AgingNexus
☰ Menu

Evidence brief · intervention

Partial reprogramming (OSK)

Synthesized from 10 indexed sources · 2026-09-11 MST · preview (no AI key)
Preview synthesis (deterministic, no AI key configured). Set a provider key to generate the full brief.

Synthesis (preview — no live AI key for the active provider):

Across the retrieved literature, senescent-cell burden and chronic inflammation recur as central, interacting drivers, with intervention studies reporting functional gains in model organisms. Key works: [1][2][3][4][5].

Set the active provider's API key to generate full model-written analysis.

Sources

  1. [1] Epigenetics in cancer
  2. [2] Bone marrow stromal cells attenuate sepsis via prostaglandin E2–dependent reprogramming of host macrophages to increase their interleukin-10 production
  3. [3] Exosomes: biogenesis, biologic function and clinical potential
  4. [4] Microglial <scp>M1/M2</scp> polarization and metabolic states
  5. [5] Hallmarks of neurodegenerative diseases
  6. [6] Aging and aging-related diseases: from molecular mechanisms to interventions and treatments
  7. [7] Autophagy in major human diseases
  8. [8] Molecular Aspects of Thyroid Hormone Actions
  9. [9] Functional rejuvenation of endothelial cell aging by transient reprogramming
  10. [10] Cellular senescence and inflammageing: from mechanisms to senotherapeutic interventions
All Partial reprogramming (OSK) works → Intervention dossier →