PIP4K2A Attenuates Cerebral Ischemia/Reperfusion Injury by Reducing the TRIB3-p62 Complex Burden and Modulating AKT/mTOR Signaling.
What this study shows
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.
At a glance
| Evidence type | A Animal model Marked A because it is an animal intervention or observation study measuring an organismal outcome (model: Mouse); the code names the system studied -- animal work can be rigorous and still not be human data. |
| Study type | 4 - Animal Study |
| Model system | Mouse |
| Journal | Translational stroke research |
| Year | 2026 |
| Peer reviewed | Yes |
| Record last updated | 2026-10-01 |
| Source | DOI 10.1007/s12975-026-01474-1 · PMID 42467322 |
Extracted findings
These fields were extracted from the paper with AI assistance and have not been checked against the source. Read them as a pointer into the paper, not as curated claims; where they disagree with the curated summary above, the curated summary stands.
| 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 |
In the Atlas
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