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Figure 6: Summary of the mechanisms of ferroptosis in AD. In the pathological context of A...
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Figure 6Figure 6
Summary of the mechanisms of ferroptosis in AD. In the pathological context of AD, glial cells are exposed to elevated levels of iron, LPS, and extracellular Aβ released from damaged neurons. i) In microglia, the expression of DMT1 and ferritin is upregulated, leading to increased intracellular iron storage. Continued iron uptake contributes to the formation of the LIP, promoting lipid peroxidation. Iron-induced ROS production activates pro-inflammatory signaling and cytokine release, which exacerbates neuroinflammation, facilitates infiltration into Aβ plaques, and enhances neuronal iron accumulation. Elevated iron levels also promote a shift toward glycolytic metabolism in microglia, reducing phagocytic capacity and accelerating Aβ deposition. Extracellular Aβ enhances ROS production via NOX, further upregulating DMT1 and iron storage, thereby establishing a vicious cycle among iron, ROS, and Aβ. ii) In astrocytes, high iron levels induce a reactive phenotype, promoting ROS generatio
▸Metadata
| doi | 10.3389/fimmu.2025.1683876 |
| pmcid | PMC12714665 |
| _origin | {'url': 'https://www.ebi.ac.uk/europepmc/articles/PMC12714665/bin/fimmu-16-1683876-g006.jpg', 'type': 'external', 'tracked_at': '2026-04-27T12:03:56.522655'} |
| caption | Summary of the mechanisms of ferroptosis in AD. In the pathological context of AD, glial cells are exposed to elevated levels of iron, LPS, and extracellular Aβ released from damaged neurons. i) In mi |
| paper_id | dabb5fb4-3d6c-460d-af8c-b4e1f8896611 |
| image_url | https://www.ebi.ac.uk/europepmc/articles/PMC12714665/bin/fimmu-16-1683876-g006.jpg |
| image_path | |
| description | |
| figure_label | Figure 6 |
| figure_number | 6 |
| _schema_version | 1 |
| source_strategy | pmc_api |
| entities_mentioned |
📊 Evidence Profile
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