MTHFD2 modulates neural stem cell proliferation and apoptosis after intracerebral hemorrhage by regulating mitochondrial NADPH homeostasis - PubMed
5 hours ago
- #Neural Stem Cells
- #Mitochondrial Redox
- #Intracerebral Hemorrhage
- MTHFD2 plays a crucial role in modulating neural stem cell (NSC) proliferation and apoptosis after intracerebral hemorrhage (ICH).
- ICH leads to initial NSC activation followed by functional exhaustion and increased apoptosis, linked to endoplasmic reticulum stress and MTHFD2 upregulation.
- MTHFD2 maintains mitochondrial integrity and redox homeostasis by regulating NADPH levels, essential for NSC survival and function.
- Knockdown of MTHFD2 reduces NSC proliferation, increases apoptosis, and worsens cognitive impairment in ICH mice.
- Exogenous NADPH supplementation partially restores NSC function, highlighting the importance of redox balance in recovery.
- Targeting mitochondrial redox metabolism via MTHFD2 could be a therapeutic strategy to improve cognitive recovery post-ICH.