ArticleJournal of the American Society of Nephrology : JASN2019
Podocyte-Specific Sialylation-Deficient Mice Serve as a Model for Human FSGS.
Article in Journal of the American Society of Nephrology : JASN, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
17 citing papers in PubMed, 25 citations in OpenAlex.
- Ultrasound-guided renal artery administration of angiopoietin-1 RNA therapy slows the progression of preclinical WT1 glomerular disease.Science translational medicine · 2026Article
- Neuraminidase activity in pediatric nephrotic syndrome.Pediatric nephrology (Berlin, Germany) · 2026Article
- Tumor sialylation regulates G-CSF stability and promotes neutrophil-mediated immunosuppression in breast cancer.Nature communications · 2026Article
- Sialic Acids in Kidney Disease: Immune Regulation, Complement Activation and Glomerular Injury.Antioxidants (Basel, Switzerland) · 2026Review
- Phase 1 Study of Oral N-Acetylmannosamine in Primary Podocytopathies.Kidney international reports · 2026Article
- Polysialic acid regulates glomerular microvasculature formation by interaction with VEGF-A188 in mice.Angiogenesis · 2025Article
- A new index for the outcome of focal segmental glomerulosclerosis.Scientific reports · 2024Article
- Resident microbes shape the vaginal epithelial glycan landscape.Science translational medicine · 2023Article
- The monosialoganglioside GM1a protects against complement attack.Cell death discovery · 2023Article
- Severe kidney dysfunction in sialidosis mice reveals an essential role for neuraminidase 1 in reabsorption.JCI insight · 2023Article
- Loss of surface transport is a main cellular pathomechanism of CRB2 variants causing podocytopathies.Life science alliance · 2023Article
- State of the art in childhood nephrotic syndrome: concrete discoveries and unmet needs.Frontiers in immunology · 2023Review
- Sulfation of sialic acid is ubiquitous and essential for vertebrate development.Scientific reports · 2022Article
- Mass spectrometry-based N-glycosylation analysis in kidney disease.Frontiers in molecular biosciences · 2022Review
- Edible Bird Nest Protects the Kidney From Gentamicin Induced Acute Tubular Necrosis.Frontiers in pharmacology · 2021Article
- Anti-apoptosis mechanism of triptolide based on network pharmacology in focal segmental glomerulosclerosis rats.Bioscience reports · 2020Article
- Cosmc-dependent mucin-typeAmerican journal of physiology. Renal physiology · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe etiology of steroid-resistant nephrotic syndrome, which manifests as FSGS, is not completely understood. Aberrant glycosylation is an often underestimated factor for pathologic processes, and structural changes in the glomerular endothelial glycocalyx have been correlated with models of nephrotic syndrome. Glycans are frequently capped by sialic acid (Sia), and sialylation's crucial role for kidney function is well known. Human podocytes are highly sialylated; however, sialylation's role in podocyte homeostasis remains unclear.
methodsWe generated a podocyte-specific sialylation-deficient mouse model (
resultsProgressive loss of sialylation in
conclusionsLoss of cell-surface sialylation in mice resulted in disturbance of podocyte homeostasis and FSGS development. Impaired podocyte adhesion to the glomerular basement membrane most likely contributed to disease development. Our data support the notion that loss of sialylation might be part of the complex process causing FSGS. Sialylation, such as through a Sia supplementation therapy, might provide a new therapeutic strategy to cure or delay FSGS and potentially other glomerulopathies.
Indexed as
Identifiers
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.