한빛사 논문
Seung Min Lee 1, Jin Woo Lee 1, Inki Kim 1 2, Dong-Cheol Woo 1 2, Chan-Gi Pack 1 2, Young Hoon Sung 1 2, In-Jeoung Baek 1 2, Chang Hee Jung 3, Young-Hak Kim 4, Chang Hoon Ha 1
1Department of Convergence Medicine and Asan Institute for Life Sciences, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea.
2Convergence Medicine Research Center (CREDIT), Asan Institute for Life Sciences, Asan Medical Center, Seoul, Republic of Korea.
3Department of Internal Medicine, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea.
4Cardiology Division, Asan Medical Center and University of Ulsan College of Medicine, Seoul, Republic of Korea.
Corresponding author. Y.-H.K.; C.H.H.
Abstract
C1q/tumor necrosis factor-related protein 9 (CTRP9) is an adipokine and has high potential as a therapeutic target. However, the role of CTRP9 in cardiovascular disease pathogenesis remains unclear. We found CTRP9 to induce HDAC7 and p38 MAPK phosphorylation via tight regulation of AMPK in vascular endothelial cells, leading to angiogenesis through increased MEF2 activity. The expression of CTRP9 and atheroprotective MEF2 was decreased in plaque tissue of atherosclerotic patients and the ventricle of post-infarction mice. CTRP9 treatment inhibited the formation of atherosclerotic plaques in ApoE KO and CTRP9 KO mice. In addition, CTRP9 induced significant ischemic injury prevention in the post-MI mice. Clinically, serum CTRP9 levels were reduced in patients with MI compared with healthy controls. In summary, CTRP9 induces a vasoprotective response via the AMPK/HDAC7/p38 MAPK pathway in vascular endothelial cells, whereas its absence can contribute to atherosclerosis and MI. Hence, CTRP9 may represent a valuable therapeutic target and biomarker in cardiovascular diseases.
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