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 ORIGINAL ARTICLE
Year : 2013  |  Volume : 61  |  Issue : 3  |  Page : 249--253

Adiponectin receptor 1 expression is associated with carotid plaque stability


1 Department of Neurosurgery, National Defense Medical College, 3-2 Namiki, Tokorozawa, Saitama, Japan
2 Department of Neurosurgery, Kamiiida Daiichi General Hospital, 2-70 Kamiiidakita-machi, Kita-ku, Nagoya, Aichi, Japan

Correspondence Address:
Satoru Takeuchi
Department of Neurosurgery, National Defense Medical College, 3-2 Namiki, Tokorozawa, Saitama 359-8513
Japan
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.115063

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Background: Adiponectin is a hormone secreted exclusively by adipose tissue, and is important in the regulation of tissue inflammation and insulin sensitivity. Adiponectin exerts its effects through two cell-surface receptors: Adiponectin receptor 1 (ADR1) and ADR2. However, the relationship between ADR1/2 expression and progression of atherosclerosis or plaque vulnerability remains unclear. Aims: To investigate the relationship between ADR1/2 expression and plaque characteristics in patients with carotid artery atherosclerosis. Materials and Methods: Forty-three patients who underwent carotid endarterectomy for treatment of carotid artery stenosis were reviewed. Immunohistochemical staining for ADR1 and ADR2 was performed in the specimens of carotid plaque. The relationships between ADR1/2 expression and clinical characteristics were analyzed statistically. Results: Plaque was stable in 7 patients and vulnerable in 36 patients. ADR1 expression was considered weak in 29 patients and strong in 14 patients. The formation of vulnerable plaques was significantly correlated with weak ADR1 expression (P < 0.003). ADR2 expression was considered weak in 14 patients and strong in 29 patients. Rates of formation of vulnerable plaque did not differ between patients with weak and strong ADR2 expression. Conclusions: Based on previous and the present results, ADR1 may be strongly related to the stabilization of established atherosclerotic plaques via inactivating macrophages. Enhancement of ADR1 expression could serve as a therapeutic target for the prevention of the formation of vulnerable plaque.






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