Tg-cut

Ciprofibrate, a fibric acid derivative, exerts its lipid-modifying effects primarily through activation of peroxisome proliferator-activated receptor alpha (PPARα), a ligand-activated nuclear receptor that regulates the expression of genes involved in lipid metabolism. Following ligand binding, PPARα forms a heterodimer with retinoid X receptor (RXR). This complex binds to specific DNA sequences known as peroxisome proliferator response elements (PPREs) in the regulatory regions of target genes, facilitating the recruitment of coactivator proteins and modulating gene transcription. PPARα activation promotes lipoprotein lipase (LPL)-mediated hydrolysis and clearance of triglyceride-rich lipoproteins. It also enhances fatty-acid uptake and β-oxidation while reducing hepatic very-low-density lipoprotein (VLDL) production, collectively contributing to lower circulating triglyceride (TG) levels. Furthermore, increased expression of apolipoproteins A-I and A-II supports HDL metabolism and contributes to increased high-density lipoprotein cholesterol (HDL-C) levels.

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