Evidence map›Paper›PMID 22367739›Full record

ArticleEMBO molecular medicine2012

Repression of miR-142 by p300 and MAPK is required for survival signalling via gp130 during adaptive hypertrophy.

Salil Sharma, Jing Liu, Jianqin Wei, Huijun Yuan, Taifang Zhang, Nanette H Bishopric

Open access · goldAbstract read
In one paragraph

Article in EMBO molecular medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed, 2 pooled it
3.2field-weighted citation impact, top 9% 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

51 citing papers in PubMed, 2 syntheses or guidelines pooled it, 101 citations in OpenAlex.

  1. Role of miRNA in Cardiovascular Diseases in Children-Systematic Review.International journal of molecular sciences · 2024
    Pooled it
  2. Pooled it
  3. Fever Inspiration: Precision Engineering for Safe and Systemic Immunotherapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Review
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  16. Review
  17. Activated CD4Aging · 2020
    Article
  18. ncRNAs in Type-2 Immunity.Non-coding RNA · 2020
    Review
  19. Article
  20. Review
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

6 authors at 1 institution in 1 country.

Salil SharmaDepartment of Molecular and Cellular Pharmacology, University of Miami Leonard M. Miller School of Medicine, Miami, FL, USA.
Jing Liu
Jianqin Wei
Huijun Yuan
Taifang Zhang
Nanette H Bishopric
University of Miami · US

Funding

Transcription Programming in Cardiac GrowthR01HL071094 · NHLBI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI BISHOPRIC, NANETTE HAHR · 2003 to 2012
$3.4M
NHLBI NIH HHS R01 HL071094NHLBI NIH HHS R-01-HL71094
6 · The paper itself

Abstract

An increase in cardiac workload, ultimately resulting in hypertrophy, generates oxidative stress and therefore requires the activation of both survival and growth signal pathways. Here, we wanted to characterize the regulators, targets and mechanistic roles of miR-142, a microRNA (miRNA) negatively regulated during hypertrophy. We show that both miRNA-142-3p and -5p are repressed by serum-derived growth factors in cultured cardiac myocytes, in models of cardiac hypertrophy in vivo and in human cardiomyopathic hearts. Levels of miR-142 are inversely related to levels of acetyltransferase p300 and MAPK activity. When present, miR-142 inhibits both survival and growth pathways by directly targeting nodal regulators p300 and gp130. MiR-142 also potently represses multiple components of the NF-κB pathway, preventing cytokine-mediated NO production and blocks translation of α-actinin. Forced expression of miR-142 during hypertrophic growth induced extensive apoptosis and cardiac dysfunction; conversely, loss of miR-142 fully rescued cardiac function in a murine heart failure model. Downregulation of miR-142 is required to enable cytokine-mediated survival signalling during cardiac growth in response to haemodynamic stress and is a critical element of adaptive hypertrophy.

Indexed as

ActininAnimalsBase SequenceCardiomegalyCells, CulturedCytokine Receptor gp130CytokinesDisease Models, AnimalDown-RegulationE1A-Associated p300 ProteinHumansMiceMicroRNAsMitogen-Activated Protein Kinase KinasesMolecular Sequence DataMyocytes, CardiacActininCytokine Receptor gp130CytokinesE1A-Associated p300 ProteinEP300 protein, humanMicroRNAsMIRN142 microRNA, humanMitogen-Activated Protein Kinase KinasesNF-kappa BNitric Oxide

Identifiers

PMID22367739
PMCPMC3407949
OpenAlexW1844216079

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.