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Figure 2.: Molecular mechanisms for glycometabolic reprogramming in microglia . Upon LPS/AT...
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Created: 2026-04-25T23:44:05
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Figure 2.Figure 2
Molecular mechanisms for glycometabolic reprogramming in microglia . Upon LPS/ATP exposure, microglia activate TLRs, which, in turn, activate AKT-mTOR signaling pathway, upregulating HIF-1α, GLUT1, and glycolysis-related enzymes (HK2, PDK, LDH). Consequently, reduced OXPHOS leads to ROS production, mitochondrial fission, and inflammatory factor secretion. Additionally, the AKT-mTOR signaling pathway directly activates NLRP3 or STAT3, promoting inflammatory transcription and further glycolysis. AMPK phosphorylation increases glucose utilization, whereas inhibition of AMPK activity induces mTOR/HIF-1α and stimulates glycolysis. LPS exposure further activates the pentose phosphate pathway, exacerbating mitochondrial dysfunction and impairing ATP production in microglia. The figure was created using www.figdraw.com and some components were assembled in Adobe Illustrator.
▸Metadata
| doi | 10.14336/AD.2023.0807 |
| pmcid | PMC11081147 |
| _origin | {'url': 'https://www.ebi.ac.uk/europepmc/articles/PMC11081147/bin/AD-15-3-1155-g2.jpg', 'type': 'external', 'tracked_at': '2026-04-26T06:44:05.644419'} |
| caption | Molecular mechanisms for glycometabolic reprogramming in microglia . Upon LPS/ATP exposure, microglia activate TLRs, which, in turn, activate AKT-mTOR signaling pathway, upregulating HIF-1α, GLUT1, an |
| paper_id | paper-ecb5be0cc3e8 |
| image_url | https://www.ebi.ac.uk/europepmc/articles/PMC11081147/bin/AD-15-3-1155-g2.jpg |
| image_path | |
| description | |
| figure_label | Figure 2. |
| figure_number | 2 |
| _schema_version | 1 |
| source_strategy | pmc_api |
| entities_mentioned |
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