Blocking the protein Ninjurin-1 in blood vessel cells reduces inflammatory signals and helps the cells survive, multiply, and move better when exposed to harmful oxidized fats.
Mechanism
Synthesis from 1 study
Bad fats trigger a protein called Ninjurin-1 to start a cycle that keeps inflammation going in blood vessel cells, which stops them from healing. When Ninjurin-1 is blocked, the inflammation cycle breaks, and the cells can survive, move, and grow again.
Most probable mechanism
When bad fats damage blood vessel cells, a protein called Ninjurin-1 turns on a harmful inflammation signal that keeps itself active and stops the cells from healing. Blocking Ninjurin-1 breaks this cycle, letting the cells survive, move, and multiply again.
Oxidized low-density lipoprotein increases expression of Ninjurin-1 in endothelial cells
Ninjurin-1 triggers phosphorylation and activation of the NF-κB p65 subunit
Activated NF-κB translocates to the nucleus and induces transcription of CXCL-8
CXCL-8 binds to its receptors on endothelial cells, reinforcing NF-κB activation through a positive feedback loop
Sustained NF-κB/CXCL-8 signaling suppresses endothelial cell proliferation and migration while promoting apoptosis
Inhibition of Ninjurin-1 disrupts this feedback loop, reducing NF-κB activation and CXCL-8 expression, thereby restoring endothelial cell survival, proliferation, and migration
Evidence from Studies
Supporting (1)
Community contributions welcome
Ninjurin-1 drives atherosclerosis progression via NF-κB/CXCL-8 activation in endothelial cells
Contradicting (0)
Community contributions welcome
Gold Standard Evidence Needed
According to GRADE and EBM methodology, here is what ideal scientific evidence would look like to definitively prove or disprove this specific claim, ordered from strongest to weakest evidence.