Tae‐Hyun Yoo
연세대학교 의과대학 · 의학
이 교수의 연구실은 만성 신장질환, 특히 신우세뇨관 섬유화와 당뇨병성 신손상의 분자 기전을 중심으로 연구를 진행하고 있습니다. Notch 신호전달 경로가 신세포 대사 재편과 관련된 PGC-1α 발현 저하를 통해 섬유화를 유도하는 메커니즘을 규명하였으며, 당뇨병성 신병변에서 순환 인자인 suPAR가 콜레스테롤 수용체인 αVβ3 인티그린을 통해 피드백으로 인한 신세포 손상을 유도하는 경로를 규명했습니다. 특히, 고형성 신증의 예후와 단백뇨 감소 양상에 대한 임상적 분석을 통해 치료 반응의 예측 가능성을 제고하고자 합니다.
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
Kidney fibrosis is the histologic manifestation of CKD. Sustained activation of developmental pathways, such as Notch, in tubule epithelial cells has been shown to have a key role in fibrosis development. The molecular mechanism of Notch-induced fibrosis, however, remains poorly understood. Here, we show that, that expression of peroxisomal proliferation g-coactivator (PGC-1<i>α</i>) and fatty acid oxidation-related genes are lower in mice expressing active Notch1 in tubular epithelial cells (Pa
Diabetic kidney disease (DKD) is the most common cause of ESRD in the United States. Podocyte injury is an important feature of DKD that is likely to be caused by circulating factors other than glucose. Soluble urokinase plasminogen activator receptor (suPAR) is a circulating factor found to be elevated in the serum of patients with FSGS and causes podocyte αVβ3 integrin-dependent migration in vitro. Furthermore, αVβ3 integrin activation occurs in association with decreased podocyte-specific exp
This study demonstrated that the prognosis of NS in IgAN was not favorable unless PR or CR was achieved. In addition, SR was more common than expected, particularly in patients with preserved kidney function and spontaneous decrease in proteinuria shortly after NS onset.
