Evidence map›Paper›PMID 18832437›Full record

ArticleJournal of the American Society of Nephrology : JASN2008

Podocyte-specific loss of functional microRNAs leads to rapid glomerular and tubular injury.

Jacqueline Ho, Kar Hui Ng, Seymour Rosen, Ales Dostal, Richard I Gregory, Jordan A Kreidberg

Open access · greenAbstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 157 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
157citing papers in PubMed, 2 pooled it
8.0field-weighted citation impact, top 3% 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

157 citing papers in PubMed, 2 syntheses or guidelines pooled it, 295 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Urinary podocyte markers in diabetic kidney disease.Kidney research and clinical practice · 2024
    Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. MicroRNAs in kidney injury and disease.Nature reviews. Nephrology · 2022
    Review
  15. The Role ofNon-coding RNA · 2022
    Article
  16. Review
  17. miRNA biomarkers in renal disease.International urology and nephrology · 2022
    Review
  18. Article
  19. Review
  20. OMICS in Chronic Kidney Disease: Focus on Prognosis and Prediction.International journal of molecular sciences · 2021
    Review

97 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 2 countries.

Jacqueline HoDepartment of Medicine, Children's Hospital Boston, 300 Longwood Avenue, Boston, MA 02115, USA.
Kar Hui Ng
Seymour Rosen
Ales Dostal
Richard I Gregory
Jordan A Kreidberg
Harvard Stem Cell Institute · USPediatrics and Genetics · USHadassah Medical Center · IL

Funding

VectorP30CA006516 · NCI · DANA-FARBER CANCER INSTITUTE · PI A. Heather Eliassen · 1985 to 2026
$330.6M
Pediatric Scientist Development Program (PSDP) [K12]K12HD000850 · NICHD · YALE UNIVERSITY · PI Sallie R. Permar · 1987 to 2026
$44.1M
NCI NIH HHS P30 CA006516NCI NIH HHS P30 CA06516NICHD NIH HHS K12 HD000850NICHD NIH HHS K12-HD00850
6 · The paper itself

Abstract

MicroRNAs (miRNAs) are in a class of endogenous, small, noncoding RNAs that exert their effects through posttranscriptional repression of specific target mRNAs. Although miRNAs have been implicated in the regulation of diverse biologic processes, little is known about miRNA function in the kidney. Here, mice lacking functional miRNAs in the developing podocyte were generated through podocyte-specific knockout of Dicer, an enzyme required for the production of mature miRNAs (Nphs2-Cre; Dicer(flx/flx)). Podocyte-specific loss of miRNAs resulted in significant proteinuria by 2 wk after birth, rapid progression of marked glomerular and tubular injury beginning at 3 wk, and death by 4 wk. Expression of the slit diaphragm proteins nephrin and podocin was decreased, and expression of the transcription factor WT1 was relatively unaffected. To identify miRNA-mRNA interactions that contribute to this phenotype, we profiled the glomerular expression of miRNAs; three miRNAs expressed in glomeruli were identified: mmu-miR-23b, mmu-miR-24, and mmu-miR-26a. These results suggest that miRNA function is dispensable for the initial development of glomeruli but is critical to maintain the glomerular filtration barrier.

Indexed as

AnimalsBase SequenceDEAD-box RNA HelicasesDNA PrimersEndoribonucleasesGene ExpressionKidney GlomerulusKidney TubulesMiceMice, KnockoutMicroRNAsPhenotypePodocytesRibonuclease IIIDEAD-box RNA HelicasesDicer1 protein, mouseDNA PrimersEndoribonucleasesMicroRNAsRibonuclease III

Identifiers

PMID18832437
PMCPMC2573018
OpenAlexW2142946696

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.