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Related Concept Videos

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Related Experiment Video

Updated: Jul 4, 2026

Flow Cytometric Analysis of Mitochondrial Reactive Oxygen Species in Murine Hematopoietic Stem and Progenitor Cells and MLL-AF9 Driven Leukemia
09:44

Flow Cytometric Analysis of Mitochondrial Reactive Oxygen Species in Murine Hematopoietic Stem and Progenitor Cells and MLL-AF9 Driven Leukemia

Published on: September 5, 2019

Iron overload induces ROS-mediated neural stem/progenitor cells apoptosis via mTOR pathway.

Fengchun Zhao1, Wei Quan1, Qian Zhang1

  • 1Department of Neurosurgery, Southwest Hospital, Army Medical University (Third Military Medical University), Chongqing, 400038, China.

BMC Neuroscience
|July 3, 2026
PubMed
Summary

Iron overload after intracerebral hemorrhage (ICH) causes neural stem/progenitor cell (NSPC) death. This occurs via increased reactive oxygen species (ROS) and altered mTOR/AMPK signaling, highlighting potential therapeutic targets.

Keywords:
Intracerebral hemorrhageIronMitochondriaNeural stem/progenitor cellsReactive oxygen species

Related Experiment Videos

Last Updated: Jul 4, 2026

Flow Cytometric Analysis of Mitochondrial Reactive Oxygen Species in Murine Hematopoietic Stem and Progenitor Cells and MLL-AF9 Driven Leukemia
09:44

Flow Cytometric Analysis of Mitochondrial Reactive Oxygen Species in Murine Hematopoietic Stem and Progenitor Cells and MLL-AF9 Driven Leukemia

Published on: September 5, 2019

Area of Science:

  • Neuroscience
  • Cell Biology
  • Biochemistry

Background:

  • Intracerebral hemorrhage (ICH) is a major cause of death and disability.
  • Iron overload is a known damaging factor following ICH.
  • The specific effects of iron overload on neural stem/progenitor cells (NSPCs) and the mechanisms involved are not well understood.

Purpose of the Study:

  • To investigate the impact of iron overload on NSPCs after ICH.
  • To elucidate the underlying molecular mechanisms of iron overload-induced NSPC death.

Main Methods:

  • In vitro study using NSPCs exposed to varying iron concentrations.
  • Assessment of cell viability, apoptosis (caspase-3 expression), and reactive oxygen species (ROS) generation.
  • Mitochondrial integrity, mTOR, and AMPK signaling pathways were analyzed.

Main Results:

  • Iron overload significantly increased NSPC death in a dose-dependent manner.
  • Elevated ROS generation and impaired mitochondrial integrity were observed.
  • Iron overload activated mTOR signaling and reduced AMPK phosphorylation.

Conclusions:

  • Post-ICH iron overload induces NSPC death through excessive ROS generation.
  • The mTOR and AMPK signaling pathways are critical mediators of this process.
  • Targeting ROS or activating AMPK may offer neuroprotective strategies for ICH recovery.