Contribution of Homeostatic Chemokines CCL19 and CCL21 and Their Receptor CCR7 to Coronary Artery Disease

Cai, Wenzhi; Tao, Jie; Zhang, Xiaolin; Tian, Xiaoxiang; Liu, Tengfei; Feng, Xiaodong; Bai, Jing; Cao, Yan; Han, Yaling

doi:10.1161/atvbaha.113.303081

Cited by 39 publications

(34 citation statements)

References 30 publications

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“…CCR7 and its ligands, Chemokine (CC-motif) ligand 19 (CCL19) and 21 (CCL21) have been associated with increased monocyte migration and are associated with increased CVD risk in humans. 34 CCR2, the receptor for monocyte chemo-attractant protein-1 (MCP-1), also enhances chemotaxis 35 and is important in the process of plaque formation in mice. 36 In our study, monocytes of patients with CKD also showed enhanced migratory capacity compared with healthy controls, suggesting that expression of these chemokine receptors in humans may also contribute to the inflammatory status of the arterial wall.…”

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confidence: 99%

Arterial and Cellular Inflammation in Patients with CKD

Moens

Verweij

Valk

et al. 2016

JASN

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CKD associates with a 1.5- to 3.5-fold increased risk for cardiovascular disease. Both diseases are characterized by increased inflammation, and in patients with CKD, elevated C-reactive protein level predicts cardiovascular risk. In addition to systemic inflammation, local arterial inflammation, driven by monocyte-derived macrophages, predicts future cardiovascular events in the general population. We hypothesized that subjects with CKD have increased arterial and cellular inflammation, reflected by F-fluorodeoxyglucose (F-FDG) positron emission tomography computed tomography (PET/CT) of the arterial wall and a migratory phenotype of monocytes. We assessed F-FDG uptake in the arterial wall in 14 patients with CKD (mean±SD age: 59±5 years, mean±SD eGFR: 37±12 ml/min per 1.73 m) but without cardiovascular diseases, diabetes, or inflammatory conditions and in 14 control subjects (mean age: 60±11 years, mean eGFR: 86±16 ml/min per 1.73 m). Compared with controls, patients with CKD showed increased arterial inflammation, quantified as target-to-background ratio (TBR) in the aorta (TBR: CKD, 3.14±0.70 versus control, 2.12±0.27; =0.001) and the carotid arteries (TBR: CKD, 2.45±0.65 versus control, 1.66±0.27; <0.001). Characterization of circulating monocytes using flow cytometry revealed increased chemokine receptor expression and enhanced transendothelial migration capacity in patients with CKD compared with controls. In conclusion, this increased arterial wall inflammation, observed in patients with CKD but without overt atherosclerotic disease and with few traditional risk factors, may contribute to the increased cardiovascular risk associated with CKD. The concomitant elevation of monocyte activity may provide novel therapeutic targets for attenuating this inflammation and thereby preventing CKD-associated cardiovascular disease.

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confidence: 99%

Arterial and Cellular Inflammation in Patients with CKD

Moens

Verweij

Valk

et al. 2016

JASN

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“…For example, CCL19/CCL21-CCR7 axis were associated with risk for coronary artery disease in a Chinese population. 80 …”

Section: Inflammation In Atherosclerosismentioning

confidence: 99%

Atherosclerosis

Lü

Daugherty

2015

ATVB

135

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Summary Mechanistic studies over the past decades using in vitro systems, animal models, and human tissues have highlighted the complexity of pathophysiological processes of atherosclerosis. Hypercholesterolemia, as one of the major risk factors for the development and progression of atherosclerosis, is still the focus of many mechanistic studies and the major therapeutic target of atherosclerosis. Although there is a dire need to validate many experimental findings in humans, there is a large number of approaches that have been showing promise for contributing to future therapeutic strategies.

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“…It was also noted that CCL19 influences the activation of leukocytes, lipid uptake of macrophages, and foam cell formation within atherosclerotic plaques. In a recent human coronary atherosclerotic plaque study, 41 immunohistochemical staining of plaques showed CCL19 expression in all stages of atherosclerosis, although levels increased with the development of atherosclerosis. It was also noted that CCL19 was expressed within endothelial cells (EC) and EC dysfunction is the initiation of atherosclerotic development.…”

Section: Discussionmentioning

confidence: 88%