ACE2 Activation in Intestinal Epithelial Cells Prevents Radiation-Induced Intestinal Injury - PubMed
4 hours ago
- #radiation-induced intestinal injury
- #MAPK/NF-κB pathways
- #ACE2
- ACE2 activation in intestinal epithelial cells (IECs) prevents radiation-induced intestinal injury (RIII).
- Diminazene aceturate (DIZE), an ACE2 agonist, blocks intestinal stem cell death and enhances crypt regeneration post-radiation.
- DIZE preserves epithelial barrier integrity and reduces intestinal inflammation, improving survival in mice.
- The radioprotective effects of DIZE are reversed by ACE2 or MasR antagonists.
- DIZE directly targets IECs, inhibiting radiation-induced MAPK (p38/JNK) and NF-κB pathways.
- ACE2 knockdown in human intestinal epithelial cells (HIECs) abolishes DIZE's protective effects.
- DIZE does not inhibit endothelial cell apoptosis or affect tumor radiosensitivity.
- First study showing selective ACE2-mediated intestinal protection without compromising tumor radiosensitivity.