ReviewNature reviews. Nephrology2010
Glomerular diseases: genetic causes and future therapeutics.
Review in Nature reviews. Nephrology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
30 citing papers in PubMed, 57 citations in OpenAlex.
- An ultrathin membrane mediates tissue-specific morphogenesis and barrier function in a human kidney chip.Science advances · 2024Article
- Assessing the effects of aging on the renal endothelial cell landscape using single-cell RNA sequencing.Frontiers in genetics · 2023Article
- Sulfatase 2 Is Associated with Steroid Resistance in Childhood Nephrotic Syndrome.Journal of clinical medicine · 2021Article
- Review
- Ste20-like kinase, SLK, a novel mediator of podocyte integrity.American journal of physiology. Renal physiology · 2018Article
- Successful production of genome-edited rats by the rGONAD method.BMC biotechnology · 2018Article
- The genetics of atypical hemolytic uremic syndrome.Medizinische Genetik : Mitteilungsblatt des Berufsverbandes Medizinische Genetik e.V · 2018Review
- RNA-seq of serial kidney biopsies obtained during progression of chronic kidney disease from dogs with X-linked hereditary nephropathy.Scientific reports · 2017Article
- Endoplasmic reticulum stress, the unfolded protein response and autophagy in kidney diseases.Nature reviews. Nephrology · 2017Review
- Thrombin-Induced Podocyte Injury Is Protease-Activated Receptor Dependent.Journal of the American Society of Nephrology : JASN · 2017Article
- Deletion of inositol-requiring enzyme-1α in podocytes disrupts glomerular capillary integrity and autophagy.Molecular biology of the cell · 2017Article
- Stress Signal Network between Hypoxia and ER Stress in Chronic Kidney Disease.Frontiers in physiology · 2017Review
- Genetic Ablation of Calcium-independent Phospholipase A2γ Induces Glomerular Injury in Mice.The Journal of biological chemistry · 2016Article
- Podocytes.F1000Research · 2016Review
- Sirtuin1 Maintains Actin Cytoskeleton by Deacetylation of Cortactin in Injured Podocytes.Journal of the American Society of Nephrology : JASN · 2015Article
- Angiotensin II induces endoplasmic reticulum stress in podocyte, which would be further augmented by PI3-kinase inhibition.Clinical hypertension · 2015Article
- MAGI-2 scaffold protein is critical for kidney barrier function.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Using zebrafish to study podocyte genesis during kidney development and regeneration.Genesis (New York, N.Y. : 2000) · 2014Review
- Proteostasis in endoplasmic reticulum--new mechanisms in kidney disease.Nature reviews. Nephrology · 2014Review
- Next-generation sequencing to dissect hereditary nephrotic syndrome in mice identifies a hypomorphic mutation in Lamb2 and models Pierson's syndrome.The Journal of pathology · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The glomerulus consists of capillary tufts, a mesangial cell component and the Bowman capsule. The glomerular filtration barrier is composed of glomerular endothelial cells, a basement membrane, and podocytes. Particular components of the slit diaphragm and the glomerular basement membrane strictly orchestrate the integrity of the glomerular filtration barrier. The basement membrane is made of a highly crosslinked macromolecular meshwork of type IV collagen, proteoglycans, and laminin. Genetic forms of glomerular disease are predominantly caused by genetic defects in these molecular structures or in factors that regulate the glomerular filtration barrier. In addition, abnormal IgA1 glycosylation can increase susceptibility to IgA nephropathy. Dysregulation of the complement system or of platelet activation can lead to the development of endocapillary lesions, which manifest as thrombotic microangiopathy. Glomerular dysfunction is also encountered in several genetic metabolic and mitochondrial disorders. Discoveries of mutations in a range of genes have provided new insights into the mechanisms of glomerular disease. In this Review, we summarize recent progress in the genetics and therapeutics of a number of glomerular diseases.
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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.