ArticleThe American journal of pathology2011
Ubiquitin C-terminal hydrolase-l1 activity induces polyubiquitin accumulation in podocytes and increases proteinuria in rat membranous nephropathy.
Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 54 citations in OpenAlex.
- Identification of conserved gene expression changes across common glomerular diseases by spatial transcriptomics.Journal of nephrology · 2025Article
- Pathogenesis of Focal Segmental Glomerulosclerosis and Minimal Change Disease: Insights from Glomerular Proteomics.Life (Basel, Switzerland) · 2025Article
- The proteasome modulates endocytosis specifically in glomerular cells to promote kidney filtration.Nature communications · 2024Article
- Cytoskeleton Rearrangement in Podocytopathies: An Update.International journal of molecular sciences · 2024Review
- Non-functional ubiquitin C-terminal hydrolase L1 drives podocyte injury through impairing proteasomes in autoimmune glomerulonephritis.Nature communications · 2023Article
- Ubiquitin C‑terminal hydrolase‑L1: A new cancer marker and therapeutic target with dual effects (Review).Oncology letters · 2023Review
- Comparative proteomic analysis of glomerular proteins in primary and bucillamine-induced membranous nephropathy.Clinical proteomics · 2022Article
- Urinary Protein and Peptide Markers in Chronic Kidney Disease.International journal of molecular sciences · 2021Review
- Lysosome function in glomerular health and disease.Cell and tissue research · 2021Review
- Role of A20/TNFAIP3 deficiency in lupus nephritis in MRL/lpr mice.Clinical and experimental nephrology · 2020Article
- Differential Expression of Urinary Exosomal Small RNAs in Idiopathic Membranous Nephropathy.BioMed research international · 2020Article
- Podocytes Produce and Secrete Functional Complement C3 and Complement Factor H.Frontiers in immunology · 2020Article
- Molecular stratification of idiopathic nephrotic syndrome.Nature reviews. Nephrology · 2019Review
- The ubiquitin-proteasome system in kidney physiology and disease.Nature reviews. Nephrology · 2019Review
- Membranous Nephropathy and Anti-Podocytes Antibodies: Implications for the Diagnostic Workup and Disease Management.BioMed research international · 2018Review
- Endoplasmic reticulum stress, the unfolded protein response and autophagy in kidney diseases.Nature reviews. Nephrology · 2017Review
- Blockage of the lysosome-dependent autophagic pathway contributes to complement membrane attack complex-induced podocyte injury in idiopathic membranous nephropathy.Scientific reports · 2017Article
- UCH-L1 Expressed by Podocytes: a Potentially Therapeutic Target for Lupus Nephritis?Inflammation · 2017Review
- Wnt/β-Catenin Signaling Mediated-UCH-L1 Expression in Podocytes of Diabetic Nephropathy.International journal of molecular sciences · 2016Article
- Ubiquitin C-terminal hydrolase 1: A novel functional marker for liver myofibroblasts and a therapeutic target in chronic liver disease.Journal of hepatology · 2015Article
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ubiquitin C-terminal hydrolase L1 (UCH-L1), a key protease of the ubiquitin-proteasome system (UPS), is associated with neurodegenerative diseases and cancer. Recently, de novo expression of UCH-L1 was described in podocytes in patients with membranous nephropathy (MN), in which UCH-L1 expression correlated with increased ubiquitin content. The objective of the present study was to investigate the role of UCH-L1 in ubiquitin homeostasis and proteasomal degradation in a rat model of MN. After disease induction, UCH-L1 expression increased in podocytes and coincided with decreased glomerular monoubiquitin content. After an initial increase in proteasomal activity, the UPS was impaired. In addition to an increase of ubiquitin in podocytes, aggregates were observed 1 year after disease induction, as in MN in human beings. Inhibition of UCH-L1 hydrolase function in MN reduced UPS impairment and ameliorated proteinuria. In contrast, inhibition of proteasomal activity enhanced UPS impairment, resulting in increased proteinuria. Stable UCH-L1 overexpression in cultured podocytes resulted in accumulation of monoubiquitin and polyubiquitin proteins. In contrast, stable knock-down of UCH-L1 reduced monoubiquitin and polyubiquitin proteins and significantly increased proteasomal activity, indicating that the observed effects in rat MN also occurred in cultured podocytes. These data demonstrate that UCH-L1 activity results in polyubiquitin accumulation, proteasome inhibition, and disease aggravation in experimental models of MN.
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