ArticleThe Journal of biological chemistry2011
MicroRNA-29c is a signature microRNA under high glucose conditions that targets Sprouty homolog 1, and its in vivo knockdown prevents progression of diabetic nephropathy.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 157 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
157 citing papers in PubMed, 1 synthesis or guideline pooled it, 265 citations in OpenAlex.
- Identification of candidate microRNA biomarkers in diabetic nephropathy: a meta-analysis of profiling studies.Journal of nephrology · 2018Pooled it
- Mir-29 repression in bladder outlet obstruction contributes to matrix remodeling and altered stiffness.PloS one · 2013Trial
- Exercise reverses diabetes-induced microRNA dysregulation in white adipose tissue.Irish journal of medical science · 2026Article
- Understanding the Roles of Non-coding RNAs and Exosomal Non-Coding RNAs in Diabetic Nephropathy.Current molecular medicine · 2025Review
- Bioinformatics analysis of miRNAs germacrone protection on diabetic nephropathy.Scientific reports · 2024Article
- Gallic Acid Alleviates Glucolipotoxicity-Induced Nephropathy by miR-709-NFE2L2 Pathway in db/db Mice on a High-Fat Diet.Journal of agricultural and food chemistry · 2024Article
- Molecular Therapeutics for Diabetic Kidney Disease: An Update.International journal of molecular sciences · 2024Review
- Research progress on miR-124-3p in the field of kidney disease.BMC nephrology · 2024Review
- Urinary podocyte markers in diabetic kidney disease.Kidney research and clinical practice · 2024Article
- Influence of Different Glucose Concentrations on the Expression of miR-29c-3p microRNA in Mesenchymal Stem Cells.International journal of hematology-oncology and stem cell research · 2024Article
- Metabolic memory: mechanisms and diseases.Signal transduction and targeted therapy · 2024Review
- MicroRNA-29b Plays a Vital Role in Podocyte Injury and Glomerular Diseases through Inducing Mitochondrial Dysfunction.International journal of biological sciences · 2024Article
- Research progress onFrontiers in pharmacology · 2024Review
- Article
- The Role of MicroRNA in the Pathogenesis of Diabetic Nephropathy.International journal of molecular sciences · 2023Review
- Pediatric Diabetic Nephropathy: Novel Insights from microRNAs.Journal of clinical medicine · 2023Article
- Extracellular vesicles metabolic changes reveals plasma signature in stage-dependent diabetic kidney disease.Renal failure · 2022Article
- On the Relationship between Diabetes and Obstructive Sleep Apnea: Evolution and Epigenetics.Biomedicines · 2022Review
- Lipid-Based Nanocarriers in Renal RNA Therapy.Biomedicines · 2022Review
- The Dynamics and Plasticity of Epigenetics in Diabetic Kidney Disease: Therapeutic Applications Vis-à-Vis.International journal of molecular sciences · 2022Review
97 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
5 authors at 1 institution in 1 country.
Funding
Abstract
Although several recent publications have suggested that microRNAs contribute to the pathogenesis of diabetic nephropathy, the role of miRNAs in vivo still remains poorly understood. Using an integrated in vitro and in vivo comparative miRNA expression array, we identified miR-29c as a signature miRNA in the diabetic environment. We validated our profiling array data by examining miR-29c expression in the kidney glomeruli obtained from db/db mice in vivo and in kidney microvascular endothelial cells and podocytes treated with high glucose in vitro. Functionally, we found that miR-29c induces cell apoptosis and increases extracellular matrix protein accumulation. Indeed, forced expression of miR-29c strongly induced podocyte apoptosis. Conversely, knockdown of miR-29c prevented high glucose-induced cell apoptosis. We also identified Sprouty homolog 1 (Spry1) as a direct target of miR-29c with a nearly perfect complementarity between miR-29c and the 3'-untranslated region (UTR) of mouse Spry1. Expression of miR-29c decreased the luciferase activity of Spry1 when co-transfected with the mouse Spry1 3'-UTR reporter construct. Overexpression of miR-29c decreased the levels of Spry1 protein and promoted activation of Rho kinase. Importantly, knockdown of miR-29c by a specific antisense oligonucleotide significantly reduced albuminuria and kidney mesangial matrix accumulation in the db/db mice model in vivo. These findings identify miR-29c as a novel target in diabetic nephropathy and provide new insights into the role of miR-29c in a previously unrecognized signaling cascade involving Spry1 and Rho kinase activation.
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.