ReviewNature reviews. Nephrology2019
The ubiquitin-proteasome system in kidney physiology and disease.
Review in Nature reviews. Nephrology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
89 citing papers in PubMed, 1 synthesis or guideline pooled it, 158 citations in OpenAlex.
- The Protective Effects of the Autophagic and Lysosomal Machinery in Vascular and Valvular Calcification: A Systematic Review.International journal of molecular sciences · 2020Pooled it
- Deubiquitinating enzymes in kidney diseases: Molecular mechanisms, pathological roles and therapeutic opportunities (Review).Molecular medicine reports · 2026Review
- Proteasome inhibition alleviates proteinuria in Lmx1b knock-in mice with dysfunctional LIM domains.Nature communications · 2026Article
- Ubiquitination-Related Diagnostic Biomarkers for Diabetic Nephropathy: Insights From Multiomic Analysis, Drug Docking, and Experimental Validation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Genomic Structural Equation Modeling Reveals Cardiovascular-Kidney-Metabolic Syndrome Genetic Architecture.Journal of diabetes · 2026Article
- Dual-mechanistic regulation of podocyte pyroptosis in lupus nephritis by the AP-1 complex: transcriptional activation of NLRP3 and lactate-mediated ubiquitination inhibition.Cell communication and signaling : CCS · 2026Article
- Pellino1-mTOR/S6K1 signaling axis is a key pathogenesis for the development of polycystic kidney disease.Cell death & disease · 2026Article
- Modular FRET sensor for site-specific detection of protein arginine methylation in living cells.American journal of translational research · 2026Article
- M2 macrophages alleviate podocyte apoptosis induced by supernatant of glomerular mesangial cells with aIgA1 via targeting UCHL1.In vitro cellular & developmental biology. Animal · 2026Article
- Longitudinal Plasma Multiomics Characterization of Nephrotoxicity in Beagles Following Repeated Dosing of Enteric-Coated Propyl Gallate Tablets.ACS pharmacology & translational science · 2025Article
- Dysregulation of the ubiquitin-proteasome system in von Hippel-Lindau syndrome: molecular insights and clinical perspectives.Clinical and experimental medicine · 2025Review
- Advances in mucopolysaccharidosis research: the impact of mass spectrometry-based approaches.Clinical proteomics · 2025Review
- Degrons: defining the rules of protein degradation.Nature reviews. Molecular cell biology · 2025Review
- Elevated FBXO45 promotes TFG ubiquitination and drives lung metastasis of hepatocellular carcinoma.JHEP reports : innovation in hepatology · 2025Article
- Article
- Prospective Pilot Study of Plasma Cell-Targeted Therapy With Bortezomib in Refractory IgA Nephropathy.Kidney international reports · 2025Article
- Phospholipid scramblase 1 (PLSCR1) is a novel substrate of NEDD4-2 (NEDD4L) mediated ubiquitination.Cell death discovery · 2025Article
- The Life of a Kidney Podocyte.Acta physiologica (Oxford, England) · 2025Review
- Small intestinal γδ T17 cells promote SAE through STING/C1q-induced microglial synaptic pruning in male mice.Nature communications · 2025Article
- Clinical value of free ubiquitin in the identification of diabetic nephropathy in patients with type 2 diabetes mellitus and preliminary exploration of its protective effect.BMC nephrology · 2025Article
29 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intracellular proteins continuously turn over by degradation and synthesis in all organ tissues. Owing to its irreversible nature, protein degradation is a highly selective process to avoid irreparable breakdown of cellular constituents, thereby disrupting cellular stability, integrity and signalling. The majority of intracellular proteins are degraded by the ubiquitin-proteasome system (UPS), a multi-enzyme process that involves the covalent conjugation of ubiquitin to a substrate protein and its recognition and degradation by the core multicomponent proteolytic complex of the UPS, the proteasome. In addition to labelling misfolded, damaged, aggregation-prone and intact but unneeded proteins for proteasomal degradation, ubiquitylation regulates a multitude of cellular processes, such as transcription, translation, endocytosis, and receptor activity and subcellular localization. In addition, the proteasome generates peptides for antigen presentation in the immune system and for further degradation by peptidases to provide amino acids for protein biosynthesis and gluconeogenesis. Alterations of the UPS or of protein substrates that render them more or less susceptible to degradation are responsible for disorders associated with renal cell dysfunction. In this Review, we provide insight into the elegant and complex nature of UPS-mediated proteostasis and focus on its established and potential roles in renal cell physiology and pathophysiology.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.