ROS-responsive self-assembly of baicalin-peptide as a "Molecular Latch" to break the endothelial-to-mesenchymal transition-inflammation loop in atherosclerotic plaques - PubMed
5 hours ago
- #Atherosclerosis
- #Peptide self-assembly
- #Inflammation
- ROS-responsive self-assembly of baicalin-peptide conjugate (VRBPC) targets atherosclerotic plaques.
- VRBPC acts as a 'Molecular Latch' to disrupt the EndMT-inflammation loop in plaques.
- Mechanism involves VCAM-1 targeting, ROS-triggered self-assembly, and HSP90 competitive binding by baicalin.
- VRBPC inhibits Smad2/3 phosphorylation, reverses EndMT, and reduces inflammation in macrophages.
- In vitro and in vivo studies show VRBPC restores endothelial function and stabilizes plaques with no systemic toxicity.
- Offers a new approach for precision therapy in atherosclerosis and inflammatory vascular diseases.