PCSK9 and triple-A syndrome: oxLDL‐induced endothelial damage via LOX‐1 receptor activation is mitigated by PCSK9‐i through dual pathways: reduction of oxLDL levels inhibits endothelial apoptosis and BBB disruption and attenuation of aortic inflammation in AAA models by suppressing macrophage infiltration and MMP‐9 activity, concurrently reducing serum TNF‐α and IL‐6 (p < 0.01) while upregulating tight junction proteins (e.g., claudin‐5) to fortify BBB integrity [36].