PIP4K2A overexpression attenuates cerebral ischemia/reperfusion injury by reducing TRIB3-p62 complex burden and modulating AKT/mTOR signaling to restore autophagic flux, identifying PIP4K2A-AKT/mTOR as a neuroprotective axis in stroke.
| Evidence tier | C Animal in vivo |
| Study type | 4 - Animal Study |
| Model system | Mouse |
| Journal | Translational stroke research |
| Year | 2026 |
| Peer reviewed | Yes |
| Source | DOI 10.1007/s12975-026-01474-1 |
Ischemic stroke remains a major cause of long-term disability. Impaired autophagic flux worsens neuronal injury after ischemia. This study elucidates the role of PIP4K2A and its regulation of autophagy in cerebral ischemia/reperfusion (I/R) injury using serum proteomics and in vivo stroke models.
| Intervention | PIP4K2A overexpression |
| Target | AKT/mTOR / autophagy / TRIB3-p62 |
| Model | Mouse |
| Effect | PIP4K2A restored autophagic flux and reduced neuronal injury via AKT/mTOR modulation in I/R stroke |