Related Experiment Video
Updated: Aug 19, 2025
Minimal Invasive Surgical Procedure of Inducing Myocardial Infarction in Mice
Published on: May 4, 2015
Angiogenic adipokine C1q-TNF-related protein 9 ameliorates myocardial infarction via histone deacetylase 7-mediated
Seung Min Lee1, Jin Woo Lee1, Inki Kim1,2
1Department of Convergence Medicine and Asan Institute for Life Sciences, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea.
Insights
C1q/tumor necrosis factor-related protein 9 (CTRP9) protects blood vessels by activating specific pathways. Lower CTRP9 levels are linked to cardiovascular diseases like atherosclerosis and myocardial infarction (MI).
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Adipokine Research
Background:
- C1q/tumor necrosis factor-related protein 9 (CTRP9) is an adipokine with therapeutic potential.
- The specific role of CTRP9 in the development of cardiovascular diseases is not fully understood.
- Understanding CTRP9's function is crucial for developing new treatments for heart conditions.
Purpose of the Study:
- To elucidate the role of CTRP9 in cardiovascular disease pathogenesis.
- To investigate the molecular mechanisms by which CTRP9 influences vascular endothelial cells.
- To evaluate CTRP9 as a potential therapeutic target and biomarker for cardiovascular diseases.
Main Methods:
- Investigated CTRP9's effects on vascular endothelial cells, focusing on AMPK, HDAC7, and p38 MAPK pathways.
- Assessed the impact of CTRP9 on angiogenesis and MEF2 activity.
- Utilized mouse models (ApoE KO, CTRP9 KO) and human patient samples (atherosclerotic plaque, post-MI ventricle, serum) for analysis.
Main Results:
- CTRP9 induces HDAC7 and p38 MAPK phosphorylation via AMPK regulation in vascular endothelial cells, promoting angiogenesis.
- Expression of CTRP9 and MEF2 is reduced in atherosclerotic plaques and post-infarction mouse ventricles.
- CTRP9 administration inhibited atherosclerosis development and prevented ischemic injury in mouse models; reduced serum CTRP9 levels were observed in MI patients.
Conclusions:
- CTRP9 mediates a vasoprotective response through the AMPK/HDAC7/p38 MAPK pathway in vascular endothelial cells.
- Reduced CTRP9 levels contribute to the pathogenesis of atherosclerosis and myocardial infarction.
- CTRP9 shows promise as a therapeutic agent and diagnostic biomarker for cardiovascular diseases.
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.
Related Concept Videos
01:21Myocarditis I: Introduction
01:24Regulation of Angiogenesis and Blood Supply