Hunjoo Ha
이화여자대학교 의예과 · 의학
허준우 교수의 연구실은 당뇨병성 신손상, 특히 당뇨병성 신우병변의 발달 기전을 중심으로 산화 스트레스와 미토콘드리아 기반의 활성산소종(ROS)이 유도하는 세밀한 신호전달 경로를 규명하고 있습니다. 주로 신거미세세포와 신관상피세포를 대상으로 하여 고과당, TGF-β1, NF-κB, MCP-1 등이 관여하는 염증 및 섬유화 반응을 분석하며, 항산화 시스템(Nrf2-HO-1)과 과산화물기반 대사 이상이 신장 기능 저하에 미치는 영향을 탐구하고 있습니다. 특히 ROS의 이차 신호전달 메커니즘과 ECM의 합성·분해 균형 붕괴를 중심으로 당뇨병성 신증의 예방 및 치료 전략을 모색하고 있습니다.
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
Diabetic nephropathy is characterized by excessive deposition of extracellular matrix (ECM) in the kidney. TGF-beta1 has been identified as the key mediator of ECM accumulation in diabetic kidney. High glucose induces TGF-beta1 in glomerular mesangial and tubular epithelial cells and in diabetic kidney. Antioxidants inhibit high glucose-induced TGF-beta1 and ECM expression in glomerular mesangial and tubular epithelial cells and ameliorate features of diabetic nephropathy, suggesting that oxidat
Although high glucose (HG) has been shown to induce nuclear factor-kappaB (NF-kappaB) activation in vascular cells, the upstream regulation and the biologic significance of NF-kappaB activation in diabetic renal injury are not clear. It was, therefore, examined if HG-induced generation of reactive oxygen species (ROS) and protein kinase C (PKC) activation are involved in NF-kappaB activation in mesangial cells (MC), and the role of NF-kappaB activation in HG-induced monocyte chemoattractant prot
Mitochondrial reactive oxygen species (ROS) play an important role in diabetes complications, including diabetic nephropathy (DN). Plasma free fatty acids (FFAs) as well as glucose are increased in diabetes, and peroxisomes and mitochondria participate in FFA oxidation in an interconnected fashion. Therefore, we investigated whether deficiency of catalase, a major peroxisomal antioxidant, accelerates DN through peroxisomal dysfunction and abnormal renal FFA metabolism. Diabetes was induced by mu
Excessive deposition of extracellular matrix (ECM) in the kidney is the hallmark of diabetic nephropathy. Although the amount of ECM deposited in the kidney depends on the balance between the synthesis and degradation of ECM, the role of ECM degradation in matrix remodeling has been less well appreciated. High glucose, advanced glycation end products, angiotensin II, and TGF-beta1 all increase intracellular reactive oxygen species (ROS) in renal cells and contribute to the development and progre
Diabetic nephropathy is characterized by excessive accumulation of extracellular matrix (ECM) in the kidney. Reactive oxygen species (ROS) play a central role in the ECM synthesis and degradation in the glomeruli and tubulointerstitium leading to renal fibrosis. High glucose (HG) induces cellular ROS through protein kinase C (PKC)-dependent activation of NADPH oxidase and through mitochondrial metabolism. ROS thus generated activate signal transduction cascade (PKC, mitogen-activated protein kin
The global burden of chronic kidney disease (CKD) intertwined with cardiovascular disease has become a major health problem. Oxidative stress (OS) plays an important role in the pathophysiology of CKD. The nuclear factor erythroid 2-related factor 2 (Nrf2)-antioxidant responsive element (ARE) antioxidant system plays a critical role in kidney protection by regulating antioxidants during OS. Heme oxygenase-1 (HO-1), one of the targets of Nrf2-ARE, plays an important role in regulating OS and is p
