Evidence map›Paper›PMID 15592803›Full record

ReviewJournal of molecular medicine (Berlin, Germany)2005

Role of endogenous antisense RNA in cardiac gene regulation.

Hans Peter Luther

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of molecular medicine (Berlin, Germany), 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

12 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Non-coding RNAs: the "dark matter" of cardiovascular pathophysiology.International journal of molecular sciences · 2013
    Review
  9. Article
  10. Article
  11. Genetic approaches for changing the heart and dissecting complex syndromes.Journal of molecular and cellular cardiology · 2008
    Review
  12. Article
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

1 author at 1 institution in 1 country.

Hans Peter LutherMedical Clinic I, Department of Cardiology, Humboldt University, Charité Hospital, Ziegelstrasse 5-9, 10117 Berlin, Germany. hans-peter.luther@charite.de
Humboldt-Universität zu Berlin · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endogenous antisense RNA has been detected for a range of eukaryotic genes and now appears to be a common phenomenon in mammalian cells. Its abundance compared to levels of its complementary sense mRNA indicates that antisense RNA may be involved in posttrancriptional regulation of a gene. In general a downregulating effect on gene expression has been demonstrated or suggested. Due to the heterogeneity in origin and character of different antisense transcripts alternative functions such as stabilizing the corresponding sense transcript and being part of gene recombination must be considered. Regulation by endogenous antisense RNA has been shown for a plethora of genes, including cardiac genes, such as myosin heavy chainMHC, atrial light chain, and troponin I. There is now growing evidence that antisense transcription is involved in human disease, and it is reasonable to consider antisense as a target for intervention procedures. Here we review the progress in our understanding of as well as the controversies arising from investigating the regulatory mechanisms of antisense RNA, with special focus on cardiac genes. Finally, links between antisense transcription and heart disease and the possible use of antisense as a target of cardiac intervention procedures are discussed.

Indexed as

AnimalsGene Expression RegulationHumansMyocardiumMyosinsRNA, AntisenseRNA InterferenceTroponin IMyosinsRNA, AntisenseTroponin I

Identifiers

PMID15592803
OpenAlexW2157562568

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.