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Tubular overexpression of transforming growth factor-beta1 induces autophagy and fibrosis but not mesenchymal transition of renal epithelial cells.
TLDR
In conclusion, overexpression of TGF-beta1 in renal tubules in vivo induces interstitial proliferation, tubular autophagy, and fibrosis, but not epithelial-to-mesenchymal transition. Expand
The LIM-homeodomain transcription factor Lmx1b plays a crucial role in podocytes.
TLDR
It is demonstrated that Lmx1b regulates important steps in glomerular development and establishes a link between three hereditary kidney diseases: nail-patella syndrome, steroid-resistant nephrotic syndrome (podocin), and Alport syndrome (collagen IV alpha4). Expand
Characterizing titin's I-band Ig domain region as an entropic spring.
TLDR
It is concluded that stretches of at least 5-6 Ig domains, perhaps coinciding with known super repeat patterns of these titin modules in the I-band, may represent the unitary lengths of the wormlike chain. Expand
Podocyte bridges between the tuft and Bowman's capsule: an early event in experimental crescentic glomerulonephritis.
TLDR
It is proposed that the spreading of podocytes on the parietal basement membrane represents a lesion of theParietal epithelium and that this process initiates the proliferation of PEC to form a crescent. Expand
From segmental glomerulosclerosis to total nephron degeneration and interstitial fibrosis: a histopathological study in rat models and human glomerulopathies.
TLDR
The present study suggests that severely injured glomeruli may continue to filter with the filtrate spreading along interstitial routes, and proposes that this kind of abnormal addition of fluid to the interstitium is the essential mechanism accounting for interstitial progression of the disease. Expand
Podocyte injury underlies the progression of focal segmental glomerulosclerosis in the fa/fa Zucker rat.
TLDR
Nphron degeneration in the fa/fa Zucker rat is studied, which is considered to be a model for non-insulin-dependent diabetes mellitus, to ensure that the destructive effects remain confined to the initially affected nephron. Expand
Effects of increased renal tubular vascular endothelial growth factor (VEGF) on fibrosis, cyst formation, and glomerular disease.
TLDR
This study shows that systemic VEGF interferes with the intraglomerular cross-talk between podocytes and the endocapillary compartment, leading to severe deterioration in glomerular architecture, similar to that seen in diabetic nephropathy. Expand
Pathways to recovery and loss of nephrons in anti-Thy-1 nephritis.
The present histopathologic study of anti-Thy-1.1 models of mesangioproliferative glomerulonephritis in rats provides a structural analysis of damage development and of pathways to recovery and toExpand
Tracer studies in the rat demonstrate misdirected filtration and peritubular filtrate spreading in nephrons with segmental glomerulosclerosis.
TLDR
It is concluded that in the context of FSGS development, misdirected filtration and peritubular filtrate spreading are important damaging mechanisms that underlie the extension of glomerular injury to the corresponding tubulointerstitium, thus leading finally to degeneration of both the glomerulus and the tubule of a severely injured nephron. Expand
Development of vascular pole-associated glomerulosclerosis in the Fawn-hooded rat.
TLDR
A step-by-step sequence of histopathologic events leading from an initial glomerular injury to segmental sclerosis in the FHH rat is elucidated. Expand
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