In zebrafish with high cholesterol, the drug rosiglitazone reduces levels of certain inflammatory molecules in blood vessel cells and decreases the buildup of immune cells and fat deposits.
Mechanism
Synthesis from 1 study
This drug turns on a natural brake in blood vessel cells that stops inflammation. When the brake is engaged, fewer immune cells stick to the vessel walls, and less fat builds up inside them. All the observed effects — less inflammation, fewer immune cells, less fat — happen because this one switch...
Most probable mechanism
A drug activates a protein in blood vessel cells that normally calms inflammation. When this protein is turned back on, it stops the production of inflammatory signals, which reduces the number of immune cells sticking to the vessel walls and prevents fat from building up inside them.
A pharmacological agent binds to and activates the PPARγ receptor in endothelial cells.
Activated PPARγ restores transcriptional repression of pro-inflammatory genes, including TNF-α and IL-1β.
Reduced expression of TNF-α and IL-1β diminishes endothelial inflammatory signaling and chemokine production.
Decreased inflammatory signaling reduces the recruitment and accumulation of myeloid cells in the vascular wall.
Reduced myeloid cell presence decreases lipid retention and deposition within the vessel wall.
Evidence from Studies
Supporting (1)
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Chronological in vivo imaging reveals endothelial inflammation prior to neutrophils accumulation and lipid deposition in HCD-fed zebrafish.
Contradicting (0)
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