C1q tumor necrosis factor-related protein 9 in atherosclerosis: Mechanistic insights and therapeutic potential

Yu, Xiaohua; Zhang, Da Wei; Zheng, Xi-Long; Tang, Chao-Ke

doi:10.1016/j.atherosclerosis.2018.07.022

Cited by 34 publications

(21 citation statements)

References 97 publications

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“…Advanced atherosclerosis with thrombus is one of the main characteristics of ACS ( Libby et al, 2019 ). Furthermore, it is reported that as a chronic inflammatory disorder in the arterial wall, atherosclerosis correlates to vascular smooth muscle cell dedifferentiation, migration and proliferation, endothelial dysfunction, inflammation, foam cell formation, and insulin resistance ( Martinez et al, 2018 ; Yu et al, 2018 ). Also, vascular endothelial cell injury is one of the leading causes of plaque erosion and thrombosis formation, which ultimately contributes to the incidence and progression of ACS and atherosclerosis ( Zhu et al, 2011 ).…”

Section: Introductionmentioning

confidence: 99%

microRNA-9 Inhibits Vulnerable Plaque Formation and Vascular Remodeling via Suppression of the SDC2-Dependent FAK/ERK Signaling Pathway in Mice With Atherosclerosis

et al. 2020

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microRNAs (miRNAs or miRs) play important roles in modulating the occurrence and progression of atherosclerosis and acute coronary syndrome (ACS). Herein, this study aimed to investigate the possible role of miR-9 in the development of atherosclerosis. Initially, the differentially expressed genes associated with ACS were screened and miRNAs that regulate syndecan-2 (SDC2) were predicted using microarray analysis. Furthermore, the biological functions of miR-9 and SDC2 on aortic plaque area, proliferation of collagen fibers, Mac-3-labeled macrophages, inflammatory response, and levels of the focal adhesion kinase/extracellular signal-regulated kinase (FAK/ERK) signaling pathway-related proteins in atherosclerosis were evaluated after ectopic miR-9 expression or SDC2 depletion in ACS mice using oil red O staining, Masson’s trichrome staining, immunohistochemistry, and Western blot analysis, respectively. SDC2 was highly-expressed, while miR-9 was poorly-expressed in atherosclerosis. Additionally, miR-9 targeted SDC2 and negatively-regulated its expression. Up-regulation of miR-9 reduced aortic plaque area, the proliferation of collagen fibers, Mac-3-labeled macrophages and levels of IL-6, IL-1β, and TNF-α by suppressing SDC2 and the FAK/ERK signaling pathway, thereby ameliorating atherosclerosis in ACS mice. In conclusion, the current study provides evidence that miR-9 retards atherosclerosis by repressing SDC2 and the FAK/ERK signaling pathway, highlighting a new theoretical basis for the treatment of atherosclerosis.

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Section: Introductionmentioning

confidence: 99%

microRNA-9 Inhibits Vulnerable Plaque Formation and Vascular Remodeling via Suppression of the SDC2-Dependent FAK/ERK Signaling Pathway in Mice With Atherosclerosis

et al. 2020

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“…CTRP9 levels are 100 times more than adiponectin in the myocardium [ 15 ]. Accumulating studies reveal that CTRP9 can protect the heart by attenuating atherosclerosis, alleviating acute ischemic injury, and attenuating adverse cardiac remodeling [ 16 – 18 ]. However, whether CTRP9 levels were altered by OSA in CAD patients remains undetermined.…”

Section: Introductionmentioning

confidence: 99%

Association of C1q/TNF-Related Protein-9 (CTRP9) Level with Obstructive Sleep Apnea in Patients with Coronary Artery Disease

Jia

et al. 2020

Mediators of Inflammation

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Background. Obstructive sleep apnea (OSA) is closely related to the incidence and progression of coronary artery disease (CAD), and the mechanisms linking OSA and CAD are multifactorial. C1q/TNF-related protein-9 (CTRP9) is a novel adipokine that protects the heart against ischemic injury and ameliorates cardiac remodeling. We aimed to ascertain the clinical relevance of CTRP9 with OSA prevalence in patients with CAD. Methods. From August 2016 to March 2019, consecutive eligible patients with CAD (n=154; angina pectoris, n=88; acute myocardial infarction [AMI], n=66) underwent cardiorespiratory polygraphy. OSA was defined as an apnea-hypopnea index (AHI) ≥15 events·h−1. Plasma CTRP9 concentrations were measured by ELISA method. Results. Moderate/severe OSA was present in 89 patients (57.8%). CTRP9 levels were significantly decreased in the moderate/severe OSA group than in the no/mild OSA group (4.7 [4.1-5.2] ng/mL vs. 4.9 [4.4-6.0] ng/mL, P=0.003). The difference between groups was only observed in patients with AMI (3.0 [2.3-4.9] vs. 4.5 [3.2-7.9], P=0.009). Correlation analysis showed that CTRP9 levels were negatively correlated with AHI (r=−0.238, P=0.003) and oxygen desaturation index (r=−0.234, P=0.004) and positively correlated with left ventricular ejection fraction (r=0.251, P=0.004) in all subjects. Multivariate analysis showed that male gender (OR 3.099, 95% CI 1.029-9.330, P=0.044), BMI (OR 1.148, 95% CI 1.040-1.268, P=0.006), and CTRP9 levels (OR 0.726, 95% CI 0.592-0.890, P=0.002) were independently associated with the prevalence of moderate/severe OSA. Conclusions. Plasma CTRP9 levels were independently related to the prevalence of moderate/severe OSA in patients with CAD, suggesting that CTRP9 might play a role in the pathogenesis of CAD exacerbated by OSA.

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“…As an adipocytokine closely related to cardiovascular disease, CTRP9 expression has been detected in many human cardiovascular diseases. In an earlier study, Wang et al reported that both CTRP9 levels in serum and CTRP9 mRNA expression in epicardial adipose tissue were decreased in coronary artery disease (CAD) patients compared with non‐CAD patients (Wang et al, 2015; Yu et al, 2018). In a study of postmenopausal women, Ahmed et al (2018) found that CTRP9 levels were decreased in both T2DM and CAD and further decreased in T2DM patients with CAD.…”

Section: Discussionmentioning

confidence: 99%

C1q/TNF‐related protein‐9 is elevated in hypertension and associated with the occurrence of hypertension‐related atherogenesis

Zhou

Cheng

Wang

et al. 2021

Cell Biology International

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C1q‐tumor necrosis factor‐related protein‐9 (CTRP9) is an important adipocytokine that is closely associated with cardiovascular disease. This study aimed to detect CTRP9 expression in hypertensive patients and mice and to analyze its effects on hypertension‐related atherogenesis. First, circulating CTRP9 levels were detected in both nonhypertensive subjects and hypertensive patients. The results showed that plasma CTRP9 levels were increased in hypertension patients compared with control subjects and gradually elevated in the Grade I, Grade II, and Grade III groups. While nondipper state did not affect CTRP9 expression in hypertension patients. Hypertension patients with carotid atherosclerotic plaque (CAP) exhibited higher CTRP9 levels and the high CTRP9 group exhibited significantly higher CAP morbidity, CTRP9 levels were positively correlated with the occurrence of CAP. Then, effects of CTRP9 on angiotensin II (Ang II)‐induced endothelial dysfunction were analyzed in vitro, and the results exhibited that treatment with Ang II significantly increased CTRP9 mRNA expression in endothelial cells (ECs), and downregulation of CTRP9 expression aggravated Ang II‐induced endothelial dysfunction in ECs. Mice were infused with Ang II, and CTRP9 was also increased in Ang II‐infused mice and mainly secreted by ECs. In Ang II‐infused ApoE−/− mice, treatment with recombinant CTRP9 significantly reduced atherosclerotic area and alleviated endothelial dysfunction. In conclusion, our results may found that CTRP9 delayed the progression of hypertension‐related arteriosclerosis by alleviating endothelial dysfunction.

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C1q tumor necrosis factor-related protein 9 in atherosclerosis: Mechanistic insights and therapeutic potential

Cited by 34 publications

References 97 publications

microRNA-9 Inhibits Vulnerable Plaque Formation and Vascular Remodeling via Suppression of the SDC2-Dependent FAK/ERK Signaling Pathway in Mice With Atherosclerosis

microRNA-9 Inhibits Vulnerable Plaque Formation and Vascular Remodeling via Suppression of the SDC2-Dependent FAK/ERK Signaling Pathway in Mice With Atherosclerosis

Association of C1q/TNF-Related Protein-9 (CTRP9) Level with Obstructive Sleep Apnea in Patients with Coronary Artery Disease

C1q/TNF‐related protein‐9 is elevated in hypertension and associated with the occurrence of hypertension‐related atherogenesis

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