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Official Full Name
C1q and tumor necrosis factor related protein 9
CTRP9 stands for C1q and tumor necrosis factor related protein 9.
RP11-307N16.1; AQL1; C1QTNF9A; CTRP9; complement C1q and tumor necrosis factor-related protein 9; complement C1q and tumor necrosis factor-related protein 9A; complement C1q tumor necrosis factor-related protein 9; complement C1q tumor necrosis factor-related protein 9A; C1QTNF9; C1q and tumor necrosis factor related protein 9; MGC48915; zgc:175268; C1qntf9

Recent Research Progress

C1q-TNF-related protein-9 (CTRP9) is an adipocytokine that has the highest amino acid identity to adiponectin, is expressed in adipose tissue and functions through activating AMP-dependent kinase (AMPK). It is well known that CTRP9 has a variety of functions, including regulation of glucose and lipid metabolism, protection from ischemia-reperfusion injury, acting as an anti-inflammatory agent and preventing oxidative damage. In particular, CTRP9 has been reported to have a beneficial effect in the cardiovascular system.

CTRP9 and type 2 diabetes

CTRP9 has been shown to promote lipid metabolism, enhance insulin sensitivity and prevent cardiovascular disease. Recent studies have shown that was significantly higher in both impaired glucose tolerance (IGT) and newly diagnosed type 2 diabetes (nT2DM) than in individuals with normal glucose tolerance (NGT) patients. The level of CTRP9 in overweight/obese subjects was much higher than lean people, and the level of CTRP9 in women was also higher than in men. In addition, circulating CTRP9 levels were positively correlated with markers of obesity and insulin resistance, including body mass index, fasting blood glucose, insulin, HbA1c, a steady-state model assessment of insulin resistance and low-density lipoprotein cholesterol, which was negatively correlated with high-density lipoprotein-cholesterol and adiponectin. In conclusion, CTRP9 is closely related to insulin resistance, suggesting that CTRP9 may play an important role in the development of type 2 diabetes.

CTRP9 and atherosclerosis

Oxidized low density lipoprotein (ox-LDL) accumulation is one of the key determinants of endothelial dysfunction in many cardiovascular diseases such as atherosclerosis. Recently, studies have found that CTRP9 stimulates up-regulation of antioxidant enzymes and endothelial nitric oxide synthase (eNOS) is dependent on peroxisome proliferator-activated receptor γ co-activator 1α (PGC-1α)/AMPK signaling activation, which helps protect endothelial dysfunction from ox-LDL. CTRP9 can be used as a candidate to protect the vascular endothelium, thus providing a promising alternative for the treatment of endothelial dysfunction in atherosclerosis.

CTRP9 and myocardial infarction

CTRP9 is a novel viable cardiomyocyte cytokine with significant down-regulated expression after myocardial infarction. In vitro studies have demonstrated that CTRP9 promotes proliferation/survival of adipose derived mesenchymal stem cells (ADSCs), stimulates migration of ADSCs, and attenuates cardiomyocyte cell death through previously unrecognized signaling mechanisms. These include binding to N-cadherin, activation of extracellular regulated protein kinases (ERK)-matrix metalloproteinase 9 and ERK-nuclear factor erythrocyte-derived 2-like 2 signaling, as well as up-regulation/secretion of antioxidant proteins. These results indicate that CTRP9 is a key factor in maintaining a healthy microenvironment, promoting stem cell transplantation of infarcted myocardium, thereby improving stem cell treatment.

CTRP9 and cardiac hypertrophy

Myocardial endothelial cells may promote cardiomyocyte hypertrophy by releasing growth factors. CTRP9 is mainly derived from myocardial capillary endothelial cells. Recent studies have demonstrated the maladaptive effects of CTRP9 during cardiac stress overload, in which CTRP9 was up-regulated in the heart and serum and drives cardiac hypertrophy through a previously unrecognized ERK5-GATA4 signaling axis. In conclusion, up-regulation of CTRP9 during hypertrophic heart disease promotes maladaptive cardiac remodeling and left ventricular dysfunction and may become a future therapeutic target.

In conclusion, CTRP9 acts as the closest adiponectin paralog, has a beneficial effect on lipid and glucose metabolism and plays a key regulatory role in vasodilation, myocardial damage and vascular smooth muscle cell proliferation. Therefore, further research on CTRP9 is very necessary and valuable.


  1. Nariman Moradi1, et al. Association of circulating CTRP9 with soluble adhesion molecules and inflammatory markers in patients with type 2 diabetes mellitus and coronary artery disease. PLOS ONE, 2018.
  2. Chang Hee Jung, et al. Association of Serum C1q/TNF-Related Protein-9 Concentration With Arterial Stiffness in Subjects With Type 2 Diabetes. J Clin Endocrinol Metab, 2014, 99(12): E2477–E2484.
  3. Risa M, et al. C1q/TNF-Related Protein-9 (CTRP9) Levels Are Associated With Obesity and Decrease Following Weight Loss Surgery. J Clin Endocrinol Metab, 2016, 101(5): 2211–2217.
  4. Haijian Sun, et al. C1q/TNF-Related Protein-9 Ameliorates Ox-LDL-Induced Endothelial Dysfunction via PGC-1α/AMPK-Mediated Antioxidant Enzyme Induction. International Journal Of Molecular Sciences, 2017, 18: 1097.
  5. Qi Liu, et al. C1q/TNF-related protein 9 inhibits the cholesterol-induced Vascular smooth muscle cell phenotype switch and cell dysfunction by activating AMP-dependent kinase. Journal of Cellular and Molecular Medicine, 2017.
  6. Yan, et al. C1q/Tumor Necrosis Factor–Related Protein-9 Regulates the Fate of Implanted Mesenchymal Stem Cells and Mobilizes Their Protective Effects Against Ischemic Heart Injury via Multiple Novel Signaling Pathways. Circulation, 2017, 136: 2162–2177.
  7. Kambara, et al. C1q/Tumor Necrosis Factor-Related Protein 9 Protects against Acute Myocardial Injury through an Adiponectin Receptor I-AMPK Dependent Mechanism. Molecular and Cellular Biology, 2015, 35: 12.
  8. Appari, et al. C1q-TNF-Related Protein-9 Promotes Cardiac Hypertrophy and Failure. Circulation Research, 2017, 120: 66-77.

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