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Podometrics as a Potential Clinical Tool for Glomerular Disease ManagementGenes and podocytes - new insights into mechanisms of podocytopathyNew insights into the pathology of podocyte loss: mitotic catastropheSoluble Urokinase Receptor and the Kidney Response in Diabetes Mellitus.Claudin 1 and nephrin label cellular crescents in diabetic glomerulosclerosisGlycogen synthase kinase 3β orchestrates microtubule remodeling in compensatory glomerular adaptation to podocyte depletion.Podocyte Number in Children and Adults: Associations with Glomerular Size and Numbers of Other Glomerular Resident CellsCell cycle re-entry sensitizes podocytes to injury induced death.Glomerular Aging and Focal Global Glomerulosclerosis: A Podometric Perspective.Wnt/β-catenin signalling and podocyte dysfunction in proteinuric kidney disease.Partial podocyte replenishment in experimental FSGS derives from nonpodocyte sourcesEstimating podocyte number and density using a single histologic section.Danger control programs cause tissue injury and remodeling.Renal progenitors and childhood: from development to disorders.Immune system modulation of kidney regeneration--mechanisms and implications.A potential role for mechanical forces in the detachment of podocytes and the progression of CKD.Progenitor cells and podocyte regeneration.Causes and pathogenesis of focal segmental glomerulosclerosis.Cell cycle control in the kidney.Necroinflammation in Kidney Disease.Transcriptome-based network analysis reveals renal cell type-specific dysregulation of hypoxia-associated transcripts.Lessons from genetics: is it time to revise the therapeutic approach to children with steroid-resistant nephrotic syndrome?Just Look! Intravital Microscopy as the Best Means to Study Kidney Cell Death Dynamics.Overexpression of Myo1e in mouse podocytes enhances cellular endocytosis, migration, and adhesion.Quantifying podocyte depletion: theoretical and practical considerations.Novel Actions of Growth Hormone in Podocytes: Implications for Diabetic Nephropathy.MAD2B contributes to podocyte injury of diabetic nephropathy via inducing cyclin B1 and Skp2 accumulation.Podocyte Regeneration Driven by Renal Progenitors Determines Glomerular Disease Remission and Can Be Pharmacologically Enhanced.WT1 Is Necessary for the Proliferation and Migration of Cells of Renin Lineage Following Kidney Podocyte Depletion.Podocyte loss involves MDM2-driven mitotic catastrophe.FSGS as an Adaptive Response to Growth-Induced Podocyte Stress.Re-expression of Sall1 in podocytes protects against adriamycin-induced nephrosis.Urinary WT1-positive cells as a non-invasive biomarker of crescent formation.NMDA receptors participate in the progression of diabetic kidney disease by decreasing Cdc42-GTP activation in podocytes.Bi-nucleation of podocytes is uniformly accompanied by foot processes widening in renal disease.Podocyte Growing Pains in Adaptive FSGS.
P2860
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P2860
description
article científic
@ca
article scientifique
@fr
articol științific
@ro
articolo scientifico
@it
artigo científico
@gl
artigo científico
@pt
artigo científico
@pt-br
artikel ilmiah
@id
artikull shkencor
@sq
artículo científico
@es
name
Podocyte mitosis - a catastrophe.
@en
type
label
Podocyte mitosis - a catastrophe.
@en
prefLabel
Podocyte mitosis - a catastrophe.
@en
P2093
P2860
P1476
Podocyte mitosis - a catastrophe
@en
P2093
H-J Anders
P Romagnani
S J Shankland
P2860
P356
10.2174/1566524011307010013
10.2174/156652413804486250
P577
2013-01-01T00:00:00Z