Activating the PGC-1α/TERT Pathway by Catalpol Ameliorates Atherosclerosis via Modulating ROS Production, DNA Damage, and Telomere Function: Implications on Mitochondria and Telomere Link

Figure 9

Graphic summary for the mechanism that catalpol ameliorates atherosclerosis through modulating telomere function, DNA damage, and ROS accumulation depending on upregulating the PGC-1α/TERT pathway. In HFD-induced atherosclerosis or oxLDL-induced macrophage injury, PGC-1α and TERT protein expressions were decreased and p53 protein expression was increased. As a result, ROS overproduction (this ROS may come from NOX2 and NOX4 overexpression and PGC-1α inhibition), increased DNA damage, cell apoptosis, and telomere dysfunction occur. Catalpol enhanced PGC-1α promoter activity and increased PGC-1α expression, thereby suppressing the aforementioned process. These findings indicated a potential mechanism of catalpol on protecting from atherosclerosis. HFD: high-fat diet; oxLDL: oxidized low-density lipoprotein.