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Related Experiment Video

Updated: May 15, 2025

Author Spotlight: Tracing the Ferroptotic Signatures and Cell Death Dynamics in Medulloblastoma for Advanced Therapeutics
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Dipyridamole Acts as Clinical Ferroptosis Inhibitor to Prevent from Tissue Injury.

Xiao Zhuang1, Shuang Shi2, Shuo Liu1,3

  • 1Department of Cell Biology, School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, Jinan, 250012, China.

Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
|May 14, 2025
PubMed
Summary

Dipyridamole, a clinical drug, effectively treats organ damage by inhibiting ferroptosis, a cell death pathway. This protection relies on its interaction with SLC7A11, offering new therapeutic strategies for ferroptosis-related diseases.

Keywords:
SLC7A11dipyridamoleferroptosistissue injury

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Area of Science:

  • Biochemistry
  • Cell Biology
  • Pharmacology

Background:

  • Ferroptosis is an iron-dependent cell death mechanism implicated in tissue injury.
  • Targeting ferroptosis shows therapeutic potential, but clinical inhibitors are lacking.
  • The precise mechanisms by which existing clinical drugs affect ferroptosis in tissue injury are largely unknown.

Purpose of the Study:

  • To screen existing clinical drugs for their ability to inhibit ferroptosis and alleviate tissue injury.
  • To elucidate the molecular mechanism by which effective drugs exert their protective effects.
  • To establish dipyridamole as a potential therapeutic agent for ferroptosis-related organ damage.

Main Methods:

  • Screening of a large panel of clinical drugs for ferroptosis inhibition.
  • In vitro and in vivo models of doxorubicin (Dox) and ischemia-reperfusion (I/R) induced organ injury.
  • Western blotting and proteasome degradation assays to investigate protein interactions.
  • Genetic manipulation (deficiency) of key molecular targets.

Main Results:

  • Dipyridamole significantly attenuated Dox or I/R-induced cardiac, liver, and kidney injury.
  • Dipyridamole's protective effect was dependent on solute carrier family 7 member 11 (SLC7A11).
  • Dipyridamole down-regulated ring finger protein 126 (RNF126), an E3 ligase that targets SLC7A11 for degradation.

Conclusions:

  • Dipyridamole alleviates organ injury by suppressing ferroptosis through a mechanism involving SLC7A11.
  • The findings identify dipyridamole as a clinical compound with therapeutic potential for ferroptosis-related tissue damage.
  • This study provides novel insights into the clinical application of ferroptosis inhibitors for treating organ injury.