Evidence map›Paper›PMID 28129112›Full record

ArticleMolecular therapy : the journal of the American Society of Gene Therapy2017

Therapeutic miR-21 Silencing Ameliorates Diabetic Kidney Disease in Mice.

Malte Kölling, Tamas Kaucsar, Celina Schauerte, Anika Hübner, Angela Dettling, Joon-Keun Park, Martin Busch, Xaver Wulff, Matthias Meier, Kristian Scherf and 10 more

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 123 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
123citing papers in PubMed, 3 pooled it
6.9field-weighted citation impact, top 2% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

123 citing papers in PubMed, 3 syntheses or guidelines pooled it, 205 citations in OpenAlex.

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  18. miRNA in the Progression of Diabetic Kidney Disease: New Insight.International journal of molecular sciences · 2025
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63 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

20 authors at 4 institutions in 4 countries.

Malte KöllingInstitute of Molecular and Translational Therapeutic Strategies (IMTTS), Hanover Medical School, 30625 Hannover, Germany.
Tamas KaucsarInstitute of Pathophysiology, Semmelweis University, 1085 Budapest, Hungary.
Celina SchauerteInstitute of Molecular and Translational Therapeutic Strategies (IMTTS), Hanover Medical School, 30625 Hannover, Germany.
Anika HübnerInstitute of Molecular and Translational Therapeutic Strategies (IMTTS), Hanover Medical School, 30625 Hannover, Germany.
Angela DettlingInstitute of Molecular and Translational Therapeutic Strategies (IMTTS), Hanover Medical School, 30625 Hannover, Germany.
Joon-Keun ParkDepartment of Nephrology, Hanover Medical School, 30625 Hannover, Germany.
Martin BuschDepartment of Internal Medicine III/Nephrology, Jena University Hospital, 07747 Jena, Germany.
Xaver WulffDepartment of Internal Medicine III/Nephrology, Jena University Hospital, 07747 Jena, Germany.
Matthias MeierDepartment of Nephrology, Hanover Medical School, 30625 Hannover, Germany.
Kristian ScherfInstitute of Molecular and Translational Therapeutic Strategies (IMTTS), Hanover Medical School, 30625 Hannover, Germany.
Nóra BukoszaInstitute of Pathophysiology, Semmelweis University, 1085 Budapest, Hungary.
Gábor SzénásiInstitute of Pathophysiology, Semmelweis University, 1085 Budapest, Hungary.
Mária GodóInstitute of Pathophysiology, Semmelweis University, 1085 Budapest, Hungary.
Amit SharmaDepartment of Hematology, Hemostasis, Oncology and Stem Cell Transplantation, Hannover Medical School, 30625 Hannover, Germany.
Michael HeuserDepartment of Hematology, Hemostasis, Oncology and Stem Cell Transplantation, Hannover Medical School, 30625 Hannover, Germany.
Peter HamarInstitute of Pathophysiology, Semmelweis University, 1085 Budapest, Hungary.
Claudia BangInstitute of Molecular and Translational Therapeutic Strategies (IMTTS), Hanover Medical School, 30625 Hannover, Germany.
Hermann HallerDepartment of Nephrology, Hanover Medical School, 30625 Hannover, Germany.
Thomas ThumInstitute of Molecular and Translational Therapeutic Strategies (IMTTS), Hanover Medical School, 30625 Hannover, Germany; National Heart and Lung Institute, Imperial College London, London SW3 6NP, UK. Electronic address: thum.thomas@mh-hannover.de.
Johan M LorenzenInstitute of Molecular and Translational Therapeutic Strategies (IMTTS), Hanover Medical School, 30625 Hannover, Germany; Department of Nephrology, Hanover Medical School, 30625 Hannover, Germany; Division of Nephrology, University Hospital Zürich, 8091 Zürich, Switzerland. Electronic address: johan.lorenzen@usz.ch.
Medizinische Hochschule Hannover · DESemmelweis University · HUJena University Hospital · DEImperial College London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetic nephropathy is the main cause of end-stage renal disease. MicroRNAs are powerful regulators of the genome, and global expression profiling revealed miR-21 to be among the most highly regulated microRNAs in kidneys of mice with diabetic nephropathy. In kidney biopsies of diabetic patients, miR-21 correlated with tubulointerstitial injury. In situ PCR analysis showed a specific enrichment of miR-21 in glomerular cells. We identified cell division cycle 25a (Cdc25a) and cyclin-dependent kinase 6 (Cdk6) as novel miR-21 targets in mesangial cells. miR-21-mediated repression of Cdc25a and Cdk6 resulted in impaired cell cycle progression and subsequent mesangial cell hypertrophy. miR-21 increased podocyte motility by regulating phosphatase and tensin homolog (Pten). miR-21 antagonism in vitro and in vivo in streptozotocin-induced diabetic mice decreased mesangial expansion, interstitial fibrosis, macrophage infiltration, podocyte loss, albuminuria, and fibrotic- and inflammatory gene expression. In conclusion, miR-21 antagonism rescued various functional and structural parameters in mice with diabetic nephropathy and, thus, might be a viable option in the treatment of patients with diabetic kidney disease.

Indexed as

Gene SilencingAnimalscdc25 PhosphatasesCell Cycle CheckpointsCell MovementCluster AnalysisCyclin-Dependent Kinase 6Diabetes Mellitus, ExperimentalDiabetic NephropathiesDisease Models, AnimalFibrosisGene Expression ProfilingGene Expression RegulationInflammationKidney GlomerulusMesangial CellsCdc25a protein, mousecdc25 PhosphatasesCyclin-Dependent Kinase 6MicroRNAsMIRN21 microRNA, mousecell-cycle regulatorsdiabetic nephropathymesangial hypertrophymicroRNAmiR-21podocyte motilityTGF-β

Identifiers

PMID28129112
PMCPMC5363308
OpenAlexW2568946527

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.