In mice genetically predisposed to atherosclerosis, a protein called Ninjurin-1 is found at higher levels in the lining of blood vessels when they develop fatty plaques, especially when the mice are...
Mechanism
Synthesis from 1 study
When fat builds up in arteries, a protein called Ninjurin-1 turns on a persistent inflammation signal inside the blood vessel lining. This signal releases a chemical that keeps the inflammation going, damages the lining, and causes fatty plaques to grow. It’s a cycle that starts with fat and gets...
Most probable mechanism
When fat builds up in artery walls, a protein called Ninjurin-1 becomes more active in the inner lining of blood vessels. This protein turns on a signaling system that triggers the release of a chemical that attracts more inflammatory cells. That chemical then feeds back to keep the signaling system active, causing ongoing damage to the vessel lining, which lets more fat and debris stick to the wall and form plaques.
Ninjurin-1 protein expression increases in endothelial cells exposed to lipid-rich conditions
Ninjurin-1 activates the NF-κB signaling pathway by promoting phosphorylation of its p65 subunit
Activated NF-κB translocates to the nucleus and increases transcription of the chemokine CXCL-8 in endothelial cells
CXCL-8 binds to its receptors on endothelial cells, reactivating NF-κB and creating a self-sustaining inflammatory loop
Sustained NF-κB/CXCL-8 signaling impairs endothelial repair functions, including proliferation and migration, while increasing cell death
Endothelial dysfunction and chronic local inflammation promote lipid retention and plaque formation in the arterial wall
Evidence from Studies
Supporting (1)
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Ninjurin-1 drives atherosclerosis progression via NF-κB/CXCL-8 activation in endothelial cells
Contradicting (0)
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Gold Standard Evidence Needed
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