YKL-40 is highly expressed in the epicardial adipose tissue of patients with atrial fibrillation and associated with atrial fibrosis

Wang, Qing; Shen, Hua; Min, Jie; Gao, Yang; Li, Kai; Wang, Xi; Yang, Jie; Liang, Yin; Xu, Jibin; Xiao, Jian; Wang, Zhinong

doi:10.1186/s12967-018-1598-0

Cited by 24 publications

(19 citation statements)

References 22 publications

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“…Authors of this study also put forward that epicardial fat may be the principal source of activin A, and activin A may be the main factor mediating the profibrosis effect of epicardial fat . Furthermore, growth of other profibrosis factors, such as YKL‐40, collagen I, matrix metalloproteinases (MMPs) 2 and 7, which participated in the process of cardiac fibrosis, was also detected …”

Section: Potential Mechanisms Underlying Eat and Af Relationshipmentioning

confidence: 80%

“…YKL‐40, a novel biomarker of inflammation and fibrosis, exhibited similar expression level in serum of AF patients and control with sinus rhythm (SR) . Yet the expression of YKL‐40 mRNA in EAT was higher in AF patients than control, and was higher in EAT than subcutaneous fat and paracardial fat . Elevated collagen I expression was also observed in AF patients, and there was a linear relationship between collagen volume fraction of the atrial myocardium and YKL‐40 mRNA expression .…”

Section: Potential Mechanisms Underlying Eat and Af Relationshipmentioning

confidence: 99%

“…Yet the expression of YKL‐40 mRNA in EAT was higher in AF patients than control, and was higher in EAT than subcutaneous fat and paracardial fat . Elevated collagen I expression was also observed in AF patients, and there was a linear relationship between collagen volume fraction of the atrial myocardium and YKL‐40 mRNA expression . Another study observed that MMPs 2 and 7 enhanced fibrosis in extracellular matrix in AF patients, whereas under the condition of heart failure‐induced atrial remodeling, expression of tissue inhibitor of metalloproteinase (TIMP), a MMPs inhibitor, changes disproportionately with upregulation of MMPs .…”

Section: Potential Mechanisms Underlying Eat and Af Relationshipmentioning

confidence: 99%

Section: Potential Mechanisms Underlying Eat and Af Relationshipmentioning

confidence: 99%

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Epicardial adipose tissue and atrial fibrillation: Possible mechanisms, potential therapies, and future directions

Zhou

Wang

Chen

et al. 2019

Pacing Clinical Electrophis

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Obesity plays an important role in the pathogenesis of atrial fibrillation (AF). Recently, rather than general fat distribution, epicardial adipose tissue (EAT) gains a growing concern. EAT is the local adipose deposition between myocardium and pericardium. Accumulated evidence revealed several distinguishing characteristics of EAT. It lies contiguously with the myocardium and could infiltration into myocardium, actively secrets cytokines and adipokines mediating inflammation or remodeling, and contains abundant ganglionated plexi. Clinical research also found EAT may be an independent risk factor of AF. Volume or thickness of EAT measured on CT or MRI could be applied as a predictor of presence, severity, and recurrence of AF. Some drugs, like antidiabetic drugs and lipid-lowing drugs, show ability to reduce EAT. Additional surgical ablation of EAT was also proved that it could improve outcome of pulmonary vein isolation for AF. In present review, we summarize recent epidemic, biological, and clinical findings about EAT and its possible role in AF. K E Y W O R D S atrial fibrillation, epicardial adipose tissue, mechanisms, therapies 1 2 THE LINK BETWEEN AF, OBESITY, AND ADIPOSE TISSUE Obesity and AFObesity is an already recognized risk factor of AF. 5,6 It is usually assessed by several indicators, such as body mass index (BMI), waist circumference, waist to hip ratio, and body fat rate. Compared with nonobese people, obese individuals possess higher probability (49%) of suffering AF, which may be associated with atrial enlargement, ventricular diastolic dysfunction, and ectopic fat depot increase. 5 Furthermore, previous literature showed that every 5 kg/m 2 increase in BMI could increase about 10-30% higher risks of AF, and also indicated that every 1 kg/m 2 reduction in BMI was associated with a significant 7% reduction in the risk of AF. 7 These pieces of evidence support that obesity is closely associated with AF occurrence. However, in general, the indicators to measure obesity, such as BMI, are relatively rough to reflect excess adipose; and individuals with similar BMI may have different risks of AF. More precise measurements are needed to predict the occurrence and development of AF.

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Section: Potential Mechanisms Underlying Eat and Af Relationshipmentioning

confidence: 80%

Section: Potential Mechanisms Underlying Eat and Af Relationshipmentioning

confidence: 99%

Section: Potential Mechanisms Underlying Eat and Af Relationshipmentioning

confidence: 99%

Section: Potential Mechanisms Underlying Eat and Af Relationshipmentioning

confidence: 99%

See 2 more Smart Citations

Epicardial adipose tissue and atrial fibrillation: Possible mechanisms, potential therapies, and future directions

Zhou

Wang

Chen

et al. 2019

Pacing Clinical Electrophis

View full text Add to dashboard Cite

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“…204 Interestingly, CHI3L1 is highly expressed in the epicardial adipose tissue of patients with atrial fibrillation and associated with atrial fibrosis. 205 Even in β-thalassemia major patients CHI3L1 is shown as a promising marker of cardiovascular disease and liver siderosis. 206 In patients with chronic heart failure, high level of serum CHI3L1 is associated with higher rates of cardiac events and regarded as an independent prognostic factor.…”

Section: Urinarymentioning

confidence: 99%

Chitinase-3 like-protein-1 function and its role in diseases

Zhao

et al. 2020

Sig Transduct Target Ther

321

265

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Non-enzymatic chitinase-3 like-protein-1 (CHI3L1) belongs to glycoside hydrolase family 18. It binds to chitin, heparin, and hyaluronic acid, and is regulated by extracellular matrix changes, cytokines, growth factors, drugs, and stress. CHI3L1 is synthesized and secreted by a multitude of cells including macrophages, neutrophils, synoviocytes, chondrocytes, fibroblast-like cells, smooth muscle cells, and tumor cells. It plays a major role in tissue injury, inflammation, tissue repair, and remodeling responses. CHI3L1 has been strongly associated with diseases including asthma, arthritis, sepsis, diabetes, liver fibrosis, and coronary artery disease. Moreover, following its initial identification in the culture supernatant of the MG63 osteosarcoma cell line, CHI3L1 has been shown to be overexpressed in a wealth of both human cancers and animal tumor models. To date, interleukin-13 receptor subunit alpha-2, transmembrane protein 219, galectin-3, chemo-attractant receptor-homologous 2, and CD44 have been identified as CHI3L1 receptors. CHI3L1 signaling plays a critical role in cancer cell growth, proliferation, invasion, metastasis, angiogenesis, activation of tumor-associated macrophages, and Th2 polarization of CD4+ T cells. Interestingly, CHI3L1-based targeted therapy has been increasingly applied to the treatment of tumors including glioma and colon cancer as well as rheumatoid arthritis. This review summarizes the potential roles and mechanisms of CHI3L1 in oncogenesis and disease pathogenesis, then posits investigational strategies for targeted therapies.

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