Dysfunction of AQP7 in the periadventitial fat: A novel trigger of atherosclerosis.
Vascular adventitial lesion as a new etiological factor of atherosclerosis (AS) has been confirmed by the results of several different animal models, and some evidence supports adventitial inflammation as the main cause, but the exact mechanism is still elusive. The data from some studies confirm that some link exists between the adventitial inflammation (which also might happen in the periadventitial fat) and atherosclerotic lesions. Aquaporin7 (AQP7) as an aquaglyceroporin, which regulates the permeation of glycerol through the cell membrane and located in the adipose tissue, shows some relationship with obesity. The result of the studies about AQP7-knockout mice and different expression of AQP7 in the cutaneous abdominal adipose tissue among people with different body types proved this phenomenon. Meanwhile, some degree of dysfunction of AQP7 has been proved in the obese. Until now, no study has shown us the data on the correlation of the expression of AQP7 in the periadventitial fat with the severity of atherosclerotic lesions. It is proposed that dysfunction of AQP7 in the periadventitial fat may trigger the adventitial inflammation. Attempts to confirm this hypothesis may lead to new directions in the study of the pathogenesis of AS and the development of a novel agent for this disorder.
He
Zhi Qing
ZQ
Department of Cardiology, Second Affiliated Hospital of the Second Military Medical University, No. 415 Fengyang Road, Shanghai 200003, China.
Liang
Chun
C
Wang
Hua
H
Wu
Zong Gui
ZG
D000273:Adipose Tissue / Q000502:physiology* / Q000503:physiopathology*; D020346:Aquaporins / Q000502:physiology*; D050197:Atherosclerosis / Q000209:etiology / Q000503:physiopathology*; D006801:Humans; D007249:Inflammation; D008954:Models, Biological
C114141:AQP7 protein, human; D020346:Aquaporins