3,4-Di-O-Caffeoylquinic Acid Inhibits Angiotensin-II-Induced Vascular Smooth Muscle Cell Proliferation and Migration by Downregulating the JNK and PI3K/Akt Signaling Pathways
Figure 6
Proposed molecular target
of CQC to inhibit Ang-II-induced proliferation and/or migration
of rVSMC. Arrows indicate the main biological end points preceding
cell proliferation and migration in response to Ang II. ROS activate
hypertrophy and proliferation in VSMC. In response to the growth
factors Ang II or PDGF, ROS are endogenously produced by VSMC and
stimulate MAPKs and Akt. Our data documented that CQC inhibited
Ang-II-induced rVSMC proliferation and migration.
The anti-atherosclerotic property of CQC may act by downregulating
the Akt, JNK and in part of ERK1/2 pathways by Ang II. AT1: angiotensin
type 1 receptor; GFR: growth factor receptor; Gq: Gq protein.
