ReviewFrontiers in medicine2015
The beneficial role of retinoids in glomerular disease.
Review in Frontiers in medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.
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
31 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.
- Systemic Redox Imbalance in Chronic Kidney Disease: A Systematic Review.Oxidative medicine and cellular longevity · 2016Pooled it
- Genetic Variants Associated With Uncontrolled Blood Pressure on Thiazide Diuretic/β-Blocker Combination Therapy in the PEAR (Pharmacogenomic Evaluation of Antihypertensive Responses) and INVEST (International Verapamil-SR Trandolapril Study) Trials.Journal of the American Heart Association · 2017Trial
- Retinoic acid receptor α activity in proximal tubules prevents kidney injury and fibrosis.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Physiological Replication of the Human Glomerulus Using a Triple Culture Microphysiological System.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Vitamin A and retinoid signaling in the kidneys.Pharmacology & therapeutics · 2023Review
- TYRO3 agonist as therapy for glomerular disease.JCI insight · 2023Article
- Article
- A reference tissue atlas for the human kidney.Science advances · 2022Article
- Liposoluble vitamins A and E in kidney disease.World journal of nephrology · 2022Review
- Proteomic and metabolomic profiling of urine uncovers immune responses in patients with COVID-19.Cell reports · 2022Article
- Accelerated protocol for the differentiation of podocytes from human pluripotent stem cells.STAR protocols · 2021Article
- Article
- Disparate roles of retinoid acid signaling molecules in kidney disease.American journal of physiology. Renal physiology · 2021Review
- Current understandings in treating children with steroid-resistant nephrotic syndrome.Pediatric nephrology (Berlin, Germany) · 2021Review
- Nuclear receptors in podocyte biology and glomerular disease.Nature reviews. Nephrology · 2021Review
- Mesenchymal Stem Cells Attenuate Renal Fibrosis via Exosomes-Mediated Delivery of microRNA Let-7i-5p Antagomir.International journal of nanomedicine · 2021Article
- Soluble RARRES1 induces podocyte apoptosis to promote glomerular disease progression.The Journal of clinical investigation · 2020Article
- The yin and yang of retinoic acid signaling in kidney diseases.The Journal of clinical investigation · 2020Article
- Rabphilin involvement in filtration and molecular uptake inDisease models & mechanisms · 2020Article
- Retinoic Acid Alleviates Cisplatin-Induced Acute Kidney Injury Through Activation of Autophagy.Frontiers in pharmacology · 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
2 authors at 2 institutions in 1 country.
Funding
Abstract
The primary etiology of CKD is a direct consequence of initial dysfunction and injury of the glomerulus, the main filtration system. Podocytes are terminally differentiated epithelial cells in the glomerulus, whose major function is the maintenance of this renal filtration barrier. Podocyte injury is implicated in many glomerular diseases including focal segmental glomerular sclerosis and HIV-associated nephropathy. In many of these diseased conditions, the podocyte can either undergo dedifferentiation and proliferation, apoptosis, or cell detachment. Regardless of the initial type of injury, the podocyte ultimately loses its functional capacity to maintain the glomerular filtration barrier. Significant injury resulting in a loss of the podocytes and failure to maintain the renal filtration barrier contributes to progressive kidney disease. Consequently, therapies that prevent podocyte injury and promote their regeneration will have a major clinical impact on glomerular disease. Retinoic acid (RA), which is a derivative of vitamin A, has many cellular functions including induction of cell differentiation, regulation of apoptosis, and inhibition of inflammation and proliferation. RA is required for kidney development and is essential for cellular differentiation in the setting of podocyte injury. The mechanism by which RA directs its beneficial effects is multifactorial, ranging from its anti-inflammatory and anti-fibrotic effects to a direct effect of upregulating podocyte differentiation markers in the podocyte. The focus of this review is to provide an overview of RA in kidney development and glomerular disease. We also highlight the key mechanism(s) by which RA restores podocyte differentiation markers and ameliorates glomerular disease.
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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.