The University of Osaka · Medicine
Professor Yoshitaka Isaka's research lab focuses on the molecular mechanisms underlying progressive kidney diseases, particularly renal fibrosis and glomerulosclerosis. The lab investigates key fibrotic pathways involving growth factors such as TGF-β and PDGF, with an emphasis on their roles in extracellular matrix accumulation and cellular remodeling. Recent work also explores the interplay between uric acid metabolism, inflammasome activation, and cellular defense mechanisms like autophagy in tubular injury. The lab integrates preclinical models with translational research, including clinical trials of novel therapeutics such as phosphate binders, to advance evidence-based nephrology practice.
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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