🖼
Figure 3: Summary of the mechanisms of ferroptosis in cerebral ischemia. Following cerebra...
active
paper figure
Created: 2026-04-27T05:03:56
By: paper_figures_pipeline
Quality:
50%
🔗 External
ID: paper-fig-dabb5fb4-3d6c-460d-af8c-b4e1f8
Figure 3Figure 3
Summary of the mechanisms of ferroptosis in cerebral ischemia. Following cerebral ischemia, energy depletion impairs the clearance of excitatory neurotransmitters from the synaptic cleft, leading to the accumulation of glutamate and other excitatory signals. This excess glutamate activates AMPA receptors, promoting Na + influx into neurons. Elevated intracellular Na + levels trigger the conversion of prothrombin into active thrombin, which in turn induces phosphorylation and activation of calcium-dependent cPLA2α. Additionally, thrombin from the bloodstream may enter the brain through a compromised blood–brain barrier, further activating cPLA2α by increasing cytosolic Ca² + concentrations. Activated cPLA2α hydrolyzes membrane phospholipids at the sn-2 position to release AA. AA is then converted to AA-CoA by ACSL4 and subsequently incorporated into membrane phospholipids via LPCAT3, forming PL-AA. Under the catalytic action of ALOX15 and the Fenton reaction, PL-AA undergoes peroxida
▸Metadata
| doi | 10.3389/fimmu.2025.1683876 |
| pmcid | PMC12714665 |
| _origin | {'url': 'https://www.ebi.ac.uk/europepmc/articles/PMC12714665/bin/fimmu-16-1683876-g003.jpg', 'type': 'external', 'tracked_at': '2026-04-27T12:03:56.330320'} |
| caption | Summary of the mechanisms of ferroptosis in cerebral ischemia. Following cerebral ischemia, energy depletion impairs the clearance of excitatory neurotransmitters from the synaptic cleft, leading to t |
| paper_id | dabb5fb4-3d6c-460d-af8c-b4e1f8896611 |
| image_url | https://www.ebi.ac.uk/europepmc/articles/PMC12714665/bin/fimmu-16-1683876-g003.jpg |
| image_path | |
| description | |
| figure_label | Figure 3 |
| figure_number | 3 |
| _schema_version | 1 |
| source_strategy | pmc_api |
| entities_mentioned |
📊 Evidence Profile
Evidence Balance
+0%
Certainty
0%
Debates
0
Incoming
0
Outgoing
0
0 supporting
0 contradicting
0 neutral
Public annotations (0)Annotate on Hypothes.is →
No public annotations yet.