ArticleThe Journal of clinical investigation2015
Anti-microRNA-21 oligonucleotides prevent Alport nephropathy progression by stimulating metabolic pathways.
Article in The Journal of clinical investigation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 232 papers.
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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.
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Who cites it
232 citing papers in PubMed, 403 citations in OpenAlex.
- Targeting MicroRNA-21 in Chronic Kidney Disease: Lessons from the Lademirsen Story.Medical sciences (Basel, Switzerland) · 2026Review
- Time- and spatially resolved LNA delivery via thermally controlled SPION technology.Molecular therapy. Nucleic acids · 2026Article
- A heterobifunctional IRAK4-targeting degrader impairs myddosome signaling in acute kidney injury and ameliorates kidney fibrosis.Communications biology · 2026Article
- Advances in the study of the breast carcinoma exosomal microRNAs: From basic mechanisms to clinical applications (Review).International journal of oncology · 2026Review
- miRNAs in Glomerular Diseases: From Pathogenic Insight to Therapeutic Potential: A Narrative Review.Cells · 2026Review
- Review
- Podocyte specific exon skipping after disease onset improves kidney pathology and function in a mouse model of Alport syndrome.Scientific reports · 2025Article
- Review
- Low circulating miR-190a-5p predicts progression of chronic kidney disease.Nature communications · 2025Article
- Role of nuclear receptors, lipid metabolism, and mitochondrial function in the pathogenesis of diabetic kidney disease.American journal of physiology. Renal physiology · 2025Review
- siRNA Therapeutics for the Treatment of Hereditary Diseases and Other Conditions: A Review.International journal of molecular sciences · 2025Review
- AntimiR uptake by human proximal tubule epithelial cells is predominantly by macropinocytosis.Scientific reports · 2025Article
- Impact of Micro-RNAs as biomarkers for end-stage renal disease related to hypertension and diabetes.Scientific reports · 2025Article
- RNA Therapies in Cardio-Kidney-Metabolic Syndrome: Advancing Disease Management.Journal of cardiovascular translational research · 2025Review
- Roles of microRNAs in cardiorenal syndrome.Molecular and cellular biochemistry · 2025Review
- High-throughput 3D spheroid screens identify microRNA sensitizers for improved thermoradiotherapy in locally advanced cancers.Molecular therapy. Nucleic acids · 2025Article
- Small Extracellular Vesicles Derived From Damaged Muscle Aggravate Kidney Injury Progression.Journal of cachexia, sarcopenia and muscle · 2025Article
- The Role of miRNAs as Early Biomarkers in Obesity-Related Glomerulopathy: Implications for Early Detection and Treatment.Biomedicines · 2025Review
- Article
- Hypermethylation and suppression of microRNA219a-2 activates the ALDH1L2/GSH/PAI-1 pathway for fibronectin degradation in renal fibrosis.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
172 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
20 authors at 6 institutions in 2 countries.
Funding
Abstract
MicroRNA-21 (miR-21) contributes to the pathogenesis of fibrogenic diseases in multiple organs, including the kidneys, potentially by silencing metabolic pathways that are critical for cellular ATP generation, ROS production, and inflammatory signaling. Here, we developed highly specific oligonucleotides that distribute to the kidney and inhibit miR-21 function when administered subcutaneously and evaluated the therapeutic potential of these anti-miR-21 oligonucleotides in chronic kidney disease. In a murine model of Alport nephropathy, miR-21 silencing did not produce any adverse effects and resulted in substantially milder kidney disease, with minimal albuminuria and dysfunction, compared with vehicle-treated mice. miR-21 silencing dramatically improved survival of Alport mice and reduced histological end points, including glomerulosclerosis, interstitial fibrosis, tubular injury, and inflammation. Anti-miR-21 enhanced PPARα/retinoid X receptor (PPARα/RXR) activity and downstream signaling pathways in glomerular, tubular, and interstitial cells. Moreover, miR-21 silencing enhanced mitochondrial function, which reduced mitochondrial ROS production and thus preserved tubular functions. Inhibition of miR-21 was protective against TGF-β-induced fibrogenesis and inflammation in glomerular and interstitial cells, likely as the result of enhanced PPARα/RXR activity and improved mitochondrial function. Together, these results demonstrate that inhibition of miR-21 represents a potential therapeutic strategy for chronic kidney diseases including Alport nephropathy.
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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.