Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2022 Aug 5;9:966478. doi: 10.3389/fmolb.2022.966478

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

Copyright © 2022 Ren, Chen, Wang and Wu.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

PMC Copyright notice

Mechanism of ferroptosis following ICH by intracellular iron overload. After ICH occurs, the hematoma releases iron ions from RBC lysis, the concentration of iron ions increase around neurons and combine with transferrin (TF) to transport iron ions into cells through TF receptor (TFR)-mediated effects. Ferric ions are reduced to ferrous ions by divalent metal transporter 1 (DMT1) and accumulate in neurons, where ferrous ions induce excessive generation of lethal ROS and lipid peroxides, therefore, resulting in ferroptosis. Iron chelators (DFX, VK-28, DP, and PIH) form a chelating ferric amine with iron ions to prevent iron ions from donating electrons to oxygen to form ROS.