Yonsei University · Medicine
Professor Tae-Hyun Yoo's research lab focuses on the molecular mechanisms underlying kidney fibrosis and diabetic kidney disease, with a particular emphasis on signaling pathways such as Notch and integrin activation in renal epithelial and podocyte cells. The lab investigates metabolic reprogramming in kidney cells, including mitochondrial function and fatty acid oxidation, and explores circulating factors like suPAR in disease progression. A central theme is identifying novel therapeutic targets to prevent or reverse fibrotic and glomerular diseases. The lab integrates preclinical models with human tissue studies to translate findings into clinical applications.
Figures are computed from collected data and may differ slightly.
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.
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