Xiaotian Yu
Stroke neurology researcher who contributed to a study of how PIP4K2A limits brain injury after ischaemia and reperfusion through the TRIB3–p62 and AKT–mTOR pathways
Affiliated Suzhou Hospital of Nanjing Medical University · Stroke neurology
Xiaotian Yu is affiliated with the Department of Neurology at the Affiliated Suzhou Hospital of Nanjing Medical University, part of a clinical-neurology team that published a 2026 paper showing PIP4K2A protects against cerebral ischemia/reperfusion injury by reducing the TRIB3-p62 complex burden and modulating AKT/mTOR signaling.
No other PubMed-indexed publication was found under this exact name at this affiliation — consistent with an early-career researcher. The affiliation itself is directly confirmed from the article's own author metadata.
Milestones in the Atlas
A selection, not a full bibliography: only papers that meet the Atlas inclusion criteria.
| Year | Evidence | Study |
|---|---|---|
| 2026 | A | PIP4K2A Attenuates Cerebral Ischemia/Reperfusion Injury by Reducing the TRIB3-p62 Complex Burden and Modulating AKT/mTOR Signaling. MA2026 Co-author on the study showing PIP4K2A attenuates cerebral ischemia/reperfusion injury via TRIB3-p62 and AKT/mTOR modulation. |
Co-authors in the Atlas 4
People with a profile here who share at least one study with Xiaotian Yu.
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- Bodun Ma Neurology researcher in Suzhou and first author of a 2026 study on how the enzyme PIP4K2A protects the brain after stroke by restoring autophagy through AKT/mTOR
- Hongxuan Feng Neurologist at Suzhou Municipal Hospital and senior author of a 2026 stroke study proposing PIP4K2A as a protector of brain tissue through AKT/mTOR signalling and autophagy
- Mei Li Scientist at the Pediatrics Research Institute of Children's Hospital of Soochow University studying brain injury, who contributed to a study of how PIP4K2A protects the brain after stroke
- Shuai Yu Neurology researcher who contributed to a study showing that the lipid kinase PIP4K2A protects the brain after ischaemic stroke by relieving a block on autophagy and boosting AKT/mTOR signalling
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