ArticleDiabetologia2014
MiR-135a promotes renal fibrosis in diabetic nephropathy by regulating TRPC1.
Article in Diabetologia, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers, 3 of them syntheses that pooled it.
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Who cites it
79 citing papers in PubMed, 3 syntheses or guidelines pooled it, 134 citations in OpenAlex.
- Potential diagnostic value of microRNAs in vascular complications of diabetes: A systematic review and meta-analysis.Journal of endocrinological investigation · 2025Pooled it
- MicroRNAs Associated with Chronic Kidney Disease in the General Population and High-Risk Subgroups-A Systematic Review.International journal of molecular sciences · 2023Pooled it
- Identification of candidate microRNA biomarkers in diabetic nephropathy: a meta-analysis of profiling studies.Journal of nephrology · 2018Pooled it
- Transient receptor potential canonical (TRPC) channels in diabetes and associated complications.Channels (Austin, Tex.) · 2026Review
- Review
- Association of miR-133a With Microalbuminuria in Patients With Resistant Arterial Hypertension and Chronic Kidney Disease.Medical science monitor : international medical journal of experimental and clinical research · 2026Article
- miR-135a-5p Is a Promising Target to Prevent the Glomerulosclerosis Associated with Podocyte Developmental Toxicity in Offspring Induced by Prenatal Dexamethasone Exposure.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Article
- Impact of Micro-RNAs as biomarkers for end-stage renal disease related to hypertension and diabetes.Scientific reports · 2025Article
- Understanding the Roles of Non-coding RNAs and Exosomal Non-Coding RNAs in Diabetic Nephropathy.Current molecular medicine · 2025Review
- TRPC3 contributes to cyclophosphamide-induced cystitis progression by enhancing bladder fibrosis through activation of the TGF-β/smad pathway.Frontiers in pharmacology · 2025Article
- Non-voltage-gated CaAmerican journal of physiology. Renal physiology · 2024Review
- A Systematic Review and Meta-Analysis of microRNA Profiling Studies in Chronic Kidney Diseases.Non-coding RNA · 2024Review
- MicroRNA193a: An Emerging Mediator of Glomerular Diseases.Biomolecules · 2023Review
- Circulating microRNAs in young individuals with long-duration type 1 diabetes in comparison with healthy controls.Scientific reports · 2023Article
- Article
- LncRNA MEG3 inhibits renal fibrinoid necrosis of diabetic nephropathy via the MEG3/miR-21/ORAI1 axis.Molecular biology reports · 2023Article
- The Role of MicroRNA in the Pathogenesis of Diabetic Nephropathy.International journal of molecular sciences · 2023Review
- MiRNA-200b level in peripheral blood predicts renal interstitial injury in patients with diabetic nephropathy.Journal of medical biochemistry · 2023Article
- Ion channels and channelopathies in glomeruli.Physiological reviews · 2023Review
19 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
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aims/hypothesisThe contribution of aberrantly expressed microRNAs (miRNAs) to diabetic nephropathy in vivo is poorly understood.
methodsIntegrated comparative miRNA array profiling was used to examine the expression of serum miRNAs in patients with diabetic nephropathy. The abundance of miRNA-135a (miR-135a) was measured by real-time quantitative PCR in the serum and kidney tissues of patients with diabetic nephropathy. The luciferase assay combined with mutation and immunoblotting was used to screen and verify the bioinformatically predicted miRNAs. Ca(2+) entry or intracellular Ca(2+) ([Ca(2+)]i) was performed by imaging Fura-2/AM-loaded cells using a fluorescence microscopy system. The role of miR-135a in vivo was explored with locked nucleic acid antisense oligonucleotides.
resultsMiR-135a was markedly upregulated in serum and renal tissue from patients with diabetic nephropathy, as well from db/db mice, and this was associated with the development of microalbuminuria and renal fibrosis. Furthermore, we identified transient receptor potential cation channel, subfamily C, member 1 (TRPC1) as a target of miR-135a during renal injury. We demonstrated that overexpression of TRPC1 was able to reverse the pathological effects of miR-135a on promoting proliferation of mesangial cells and increasing synthesis of extracellular matrix proteins. Moreover, miR-135a attenuated store depletion-induced Ca(2+) entry into cells by regulating TRPC1. Importantly, knockdown of miR-135a in diabetic kidneys restored levels of TRPC1 and reduced synthesis of fibronectin and collagen I in vivo. Suppressing TRPC1 levels to prevent Ca(2+) entry into cells may be a mechanism whereby miR-135a promotes renal fibrosis in diabetic kidney injury. CONCLUSIONS/
interpretationThese findings suggest an important role for miR-135a in renal fibrosis and inhibition of miR-135a might be an effective therapy for diabetic 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.