Nagoya University · 의학
Koji Ohashi 교수의 연구실은 간비세포에서 분비되는 호르몬인 아미핀ectin의 다기능적 기능을 중심으로, 대사질환과 심혈관 질환의 발병 메커니즘을 규명하고 있습니다. 특히 아미핀ectin의 매크로파지 분화 조절, 혈압 조절, 신장 손상 보호 작용, 그리고 혈관 재생에 대한 영향을 분자생물학적·동물모델을 기반으로 연구하고 있습니다. 이는 비만, 당뇨, 고혈압 등 대사증후군 관련 질환의 새로운 치료 전략 개발에 기여하고자 하는 목적이 있습니다.
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
It is established that the adipocyte-derived cytokine adiponectin protects against cardiovascular and metabolic diseases, but the effect of this adipokine on macrophage polarization, an important mediator of disease progression, has never been assessed. We hypothesized that adiponectin modulates macrophage polarization from that resembling a classically activated M1 phenotype to that resembling alternatively-activated M2 cells. Peritoneal macrophages and the stromal vascular fraction (SVF) cells
Patients with obesity are susceptible to hypertension. We have reported that the plasma adiponectin levels are decreased in obesity and that adiponectin has many defensive properties against obesity-related diseases, such as type 2 diabetes and coronary artery disease. The aim of this study was to determine the relationship between adiponectin and hypertension in mice. We measured blood pressure and heart rate directly by a catheter in the carotid artery and indirectly by automatic sphygmomanome
Adiponectin accumulates to the injured kidney, and prevents glomerular and tubulointerstitial injury through modulating inflammation and oxidative stress.
Adiponectin is a fat-derived plasma protein that has cardioprotective roles in obesity-linked diseases. Because cyclooxygenase 2 (COX-2) is an important modulator of endothelial function, we investigated the possible contribution of COX-2 to adiponectin-mediated vascular responses in a mouse hind limb model of vascular insufficiency. Ischemic insult increased COX-2 expression in endothelial cells of wild-type mice, but this induction was attenuated in adiponectin knockout mice. Ischemia-induced
