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ACE2 Activation in Intestinal Epithelial Cells Prevents Radiation-Induced Intestinal Injury.

Xinglei Song1, Renjun Peng2, Zhongmin Chen2

  • 1The Postgraduate Training Base of Jinzhou Medical University, The Characteristic Medical Center of PLA Rocket Force, Beijing, China.

Antioxidants & Redox Signaling
|March 4, 2026
PubMed
Summary
This summary is machine-generated.

Activating the ACE2 pathway with DIZE protects intestinal stem cells from radiation damage, improving survival without affecting tumor radiosensitivity. This offers a novel strategy for radiotherapy patients.

Keywords:
ACE2MAPK/NF-κBdiminazene aceturateintestinal epithelial cellsradiation-induced intestinal injury

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Area of Science:

  • Molecular Biology
  • Radiotherapy
  • Gastroenterology

Background:

  • Radiation-induced intestinal injury (RIII) is a severe side effect of radiotherapy for abdominal/pelvic cancers.
  • The ACE2/Ang-(1-7)/MasR axis is a protective pathway with potential anti-inflammatory roles.
  • Targeting this axis may offer a novel approach to mitigate RIII.

Purpose of the Study:

  • To investigate the role of ACE2 activation in mitigating radiation-induced intestinal injury (RIII).
  • To explore the underlying mechanisms of ACE2-mediated radioprotection in the intestine.
  • To assess if ACE2 activation impacts tumor radiosensitivity.

Main Methods:

  • Mice were treated with diminazene aceturate (DIZE), a selective ACE2 agonist, prior to lethal radiation.
  • Effects on intestinal stem cells (ISCs), crypt regeneration, epithelial barrier integrity, and survival were assessed.
  • In vitro studies using human intestinal epithelial cells (HIECs) and endothelial cells were performed, along with tumor radiosensitivity assays.

Main Results:

  • DIZE treatment protected ISCs from radiation-induced death, enhanced crypt regeneration, preserved barrier integrity, and reduced inflammation, significantly improving mouse survival.
  • The radioprotective effects were dependent on ACE2 and MasR, and DIZE inhibited radiation-induced MAPK and NF-κB pathways specifically in intestinal epithelial cells.
  • DIZE did not protect endothelial cells or compromise the radiosensitivity of colorectal tumor cells in vitro or in vivo.

Conclusions:

  • ACE2 activation, via DIZE, selectively protects intestinal epithelial cells from radiation damage by inhibiting MAPK/NF-κB signaling.
  • This selective protection improves intestinal integrity and survival without compromising tumor radiosensitivity.
  • Targeting the ACE2 pathway represents a promising therapeutic strategy to alleviate RIII in cancer patients undergoing radiotherapy.