Evidence map›Paper›PMID 22367207›Full record

ArticleThe Journal of biological chemistry2012

A novel cardiomyocyte-enriched microRNA, miR-378, targets insulin-like growth factor 1 receptor: implications in postnatal cardiac remodeling and cell survival.

Ivana Knezevic, Aalok Patel, Nagalingam R Sundaresan, Mahesh P Gupta, R John Solaro, Raghu S Nagalingam, Madhu Gupta

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed, 1 pooled it
5.9field-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

79 citing papers in PubMed, 1 synthesis or guideline pooled it, 130 citations in OpenAlex.

  1. Role of miRNA in Cardiovascular Diseases in Children-Systematic Review.International journal of molecular sciences · 2024
    Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Roles of non-coding RNA in diabetic cardiomyopathy.Cardiovascular diabetology · 2024
    Review
  8. Article
  9. Article
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  11. Review
  12. Review
  13. Article
  14. Article
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  19. Article
  20. Article

19 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

7 authors at 2 institutions in 1 country.

Ivana KnezevicDepartment of Physiology and Biophysics, and Center for Cardiovascular Research, University of Illinois, Chicago, Illinois 60612, USA.
Aalok Patel
Nagalingam R Sundaresan
Mahesh P Gupta
R John Solaro
Raghu S Nagalingam
Madhu Gupta
University of Illinois Chicago · USUniversity of Chicago · US

Funding

TRAINING IN CELLULAR SIGNALLING IN THE CARDIOVASCULAR SYT32HL007692 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI SOLARO, R JOHN · 1990 to 2014
$8.5M
MODULATION OF CALCIUM CONTROL OF CARDIAC MYOFIBRILSR01HL022231 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI GUPTA, MADHU, SOLARO, R JOHN · 1985 to 2014
$2.9M
The Role of PARP-SIR2 Signaling in Heart FailureR01HL083423 · NHLBI · UNIVERSITY OF CHICAGO · PI GUPTA, MAHESH P · 2007 to 2011
$2.4M
NHLBI NIH HHS 2R01 HL 22231NHLBI NIH HHS P01 HL 062626NHLBI NIH HHS R01 HL022231NHLBI NIH HHS R01 HL083423NHLBI NIH HHS R01 HL 83423NHLBI NIH HHS T32 HL007692NHLBI NIH HHS T32 HL 07692
6 · The paper itself

Abstract

Postnatal cardiac remodeling is characterized by a marked decrease in the insulin-like growth factor 1 (IGF1) and IGF1 receptor (IGF1R) expression. The underlying mechanism remains unexplored. This study examined the role of microRNAs in postnatal cardiac remodeling. By expression profiling, we observed a 10-fold increase in miR-378 expression in 1-week-old neonatal mouse hearts compared with 16-day-old fetal hearts. There was also a 4-6-fold induction in expression of miR-378 in older (10 months) compared with younger (1 month) hearts. Interestingly, tissue distribution analysis identified miR-378 to be highly abundant in heart and skeletal muscles. In the heart, specific expression was observed in cardiac myocytes, which was inducible by a variety of stressors. Overexpression of miR-378 enhanced apoptosis of cardiomyocytes by direct targeting of IGF1R and reduced signaling in Akt cascade. The inhibition of miR-378 by its anti-miR protected cardiomyocytes against H(2)O(2) and hypoxia reoxygenation-induced cell death by promoting IGF1R expression and downstream Akt signaling cascade. Additionally, our data show that miR-378 expression is inhibited by IGF1 in cardiomyocytes. In tissues such as fibroblasts and fetal hearts, where IGF1 levels are high, we found either absent or significantly low miR-378 levels, suggesting an inverse relationship between these two factors. Our study identifies miR-378 as a new cardioabundant microRNA that targets IGF1R. We also demonstrate the existence of a negative feedback loop between miR-378, IGF1R, and IGF1 that is associated with postnatal cardiac remodeling and with the regulation of cardiomyocyte survival during stress.

Indexed as

AnimalsApoptosisBase SequenceCells, CulturedCell SurvivalGene Expression Regulation, DevelopmentalHeartHypoxiaMiceMicroRNAsMolecular Sequence DataMyocytes, CardiacProto-Oncogene Proteins c-aktRatsRats, Sprague-DawleyReceptor, IGF Type 1Akt1 protein, mouseAkt1 protein, ratMicroRNAsMIRN378 microRNA, mouseMIRN378 microRNA, ratProto-Oncogene Proteins c-aktReceptor, IGF Type 1

Identifiers

PMID22367207
PMCPMC3339988
OpenAlexW2006535542

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.