大阪大学 · 医学
伊坂義隆教授の研究室は、腎疾患の末期病態である糸 Knot硬化症や間質線維化の発症メカニズムに焦点を当て、TGF-βやPDGFといった成長因子の役割を動物モデルを用いた遺伝子導入技術で解明しています。特に、腎臓における成長因子の局所的過剰発現が線維化を引き起こすメカニズムを、分子・細胞レベルで解明しており、腎線維化の治療標的にする新規標的戦略の開発をめざしています。また、尿酸腎症における炎症小体の活性化と自己astyのバランスについても、細胞保護機構の解明を進めています。
Figures are computed from collected data and may differ slightly.
Glomerulosclerosis, a final common lesion of various glomerular diseases, is characterized by mesangial cell proliferation and extracellular matrix (ECM) expansion. TGF-beta and PDGF are known to play a critical role in the regulation of ECM metabolism and mesenchymal cell proliferation, respectively. However, there is little evidence to demonstrate the direct role of each of these growth factors in the pathogenesis of glomerulosclerosis. Using an in vivo transfection technique, we could realize
Renal fibrosis is the final common pathway of numerous progressive kidney diseases, and transforming growth factor-β (TGF-β) has an important role in tissue fibrosis by up-regulating matrix protein synthesis, inhibiting matrix degradation, and altering cell-cell interaction. Many strategies targeting TGF-β, including inhibition of production, activation, binding to the receptor, and intracellular signaling, have been developed. Some of them were examined in clinical studies against kidney fibros
Classically, urate nephropathy has been postulated to cause kidney disease by depositing intraluminal crystal in the collecting duct. Recently, molecular mechanisms of inflammasome have been investigated. Urate-induced inflammasome pathway is comprised of urate crystal uptake into intracellular lysosomes and subsequent lysosomal rupture with mitochondrial reactive oxygen species (ROS) production, which activates the NLRP3 inflammasome. Against the lysosomal rupture and mitochondrial ROS producti
Evaluate the New Phosphate Iron-Based Binder Sucroferric Oxyhydroxide in Dialysis Patients with the Goal of Advancing the Practice of EBM (EPISODE), jRCTs051180048.
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