Fig. 9
From: Cordycepin prevents radiation ulcer by inhibiting cell senescence via NRF2 and AMPK in rodents
Proposed model of cordycepin as radiation ulcer mitigator by preventing cell senescence. Persistent DNA damage foci forms and senescent cells accumulate in radiation ulcer, which involved in the development of radiation ulcer. Cordycepin activates AMPK by directly binding to AMPK protein via interacting with the α1 and γ1 subunit near the autoinhibitory domain (AID), activated AMPK promotes p62-dependent autophagic degradation of Keap1, thus, NRF2 dissociates from Keap1 and moves to the nucleus, where it transactivates ARE-containing antioxidant genes
