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Complement C1q tumor necrosis factor-related proteins1 (CTRP1) was identified as an adipokines; its expression in smooth muscle, adipose tissue, heart tissue and cardiomyocytes is high. Studies have shown that serum levels of CTRP1 were significantly elevated in patients with type 2 diabetes, hypertension, and chronic heart failure.

CTRP1 and NAFLD

Nonalcoholic fatty liver disease (NAFLD) is a chronic liver disease that accounts for a large proportion of the general population. NAFLD is closely related to the entire spectrum of metabolic-related disorders, including diabetes, obesity and cardiovascular disease. A growing body of evidence demonstrates the important role of adipokines in the context of NAFLD. Adipokines produced by different tissues, primarily fat, modulate numerous pathways including glucose and fatty acid metabolism and inflammation. Recent studies have found that CTRP1 enhanced glucose and fatty acid oxidation, improved insulin sensitivity, attenuated plaque formation, and increased aldosterone production. Therefore, various roles in the metabolic pathway can link CTRP1 to the pathogenesis of NAFLD.

CTRP1 and CAD

CTRPs have been shown to have different biological effects on the cardiovascular system. However, the correlation between CTRP1 and coronary artery disease (CAD) is rarely explored. Recently, studies by Wang et al. showed that serum CTRP1 levels were significantly elevated in CAD patients and increased with the severity of CAD. The level of CTRP1 in the acute myocardial infarction group was much higher than that in the stable/unstable angina and non-CAD groups. Significant differences in CTRP1 were also found between single vessel disease and triple-vessel disease. Multivariate logistic regression analysis showed that CTRP1 was an independent risk factor for myocardial infarction. In conclusion, elevated serum CTRP1 levels are closely related to the prevalence and severity of CAD and may be considered markers of myocardial infarction.

CTRP1 and cardiac hypertrophy

CTRP1 is expressed in the myocardium; however, its function in myocytes has not been studied. Recently, studies have shown that CTRP1 attenuates angiotensin II-induced cardiac hypertrophy by activating the AMP-activated protein kinase a (AMPKa) pathway. Some studies have shown that the anti-hypertrophic effect of CTRP1 is dependent on AMPKa activation, which inhibits mTOR P70S6K phosphorylation. The AMPKa inhibitor eliminated the anti-hypertrophic effect of the recombinant human globular domain of CTRP1 both in vivo and in vitro. Furthermore, CTRP1-mediated AMPKa activation was triggered by inhibition of PDE1-4, which subsequently activated the Cyclic AMP (cAM) P/PKA/LKB1 pathway. CTRP1 improves cardiac function and inhibits cardiac hypertrophy and fibrosis by increasing and activating AMPKa, suggesting that CTRP1 may be a therapeutic target for cardiac hypertrophy and heart failure.

CTRP1 and type 2 diabetes

CTRP1 is independently associated with type 2 diabetes. However, the relationship between CTRP1 and insulin resistance remains undetermined. Studies have shown that patients with diabetes have higher plasma CTRP1 and a negative correlation with insulin resistance. Glucose utilization tests have shown that CTRP1 can increase the glucose utilization rate of mature adipocytes in the presence of insulin. CTRP1 was not only associated with IRS-1 protein, but also negatively correlated with IRS-1 Ser1101 phosphorylation. In general, CTRP1 may improve insulin resistance by reducing phosphorylation of IRS-1 Ser1101, induced in the situation of insulin resistance as a feedback adipokine.

In summary, CTRP1, as a novel adipocytokines, may be involved in the mechanisms of metabolism and inflammation. However, the clinical relevance of CTRP1 is rarely explored. Therefore, further research to clarify the physiology and pathophysiology of CTRP1 is very necessary.