Evidence map›Paper›PMID 21838751›Full record

ArticleBritish journal of pharmacology2012

Long-term treatment with ivabradine in post-myocardial infarcted rats counteracts f-channel overexpression.

S Suffredini, F Stillitano, L Comini, M Bouly, S Brogioni, C Ceconi, R Ferrari, A Mugelli, E Cerbai

Abstract read
In one paragraph

Article in British journal of pharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

27 citing papers in PubMed, 62 citations in OpenAlex.

  1. Review
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  15. Article
  16. Article
  17. Review
  18. Treatment of inappropriate sinus tachycardia with ivabradine.Journal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing · 2016
    Review
  19. Article
  20. HCN Channels Modulators: The Need for Selectivity.Current topics in medicinal chemistry · 2016
    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

9 authors at 3 institutions in 2 countries.

S SuffrediniCenter of Molecular Medicine (C.I.M.M.B.A.), Florence, Italy.
F Stillitano
L Comini
M Bouly
S Brogioni
C Ceconi
R Ferrari
A Mugelli
E Cerbai
Fondazione Salvatore Maugeri · ITUniversity of Florence · ITServier (France) · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeRecent clinical data suggest beneficial effects of ivabradine, a specific heart rate (HR)-lowering drug, in heart failure patients. However, the mechanisms responsible for these effects have not been completely clarified. Thus, we investigated functional/molecular changes in I(f), the specific target of ivabradine, in the failing atrial and ventricular myocytes where this current is up-regulated as a consequence of maladaptive remodelling. EXPERIMENTAL APPROACH: We investigated the effects of ivabradine (IVA; 10 mg·kg(-1) ·day(-1) for 90 days) on electrophysiological remodelling in left atrial (LA), left ventricular (LV) and right ventricular (RV) myocytes from post-mycardial infarcted (MI) rats, with sham-operated (sham or sham + IVA) rats as controls. I(f) current was measured by patch-clamp; hyperpolarization-activated cyclic nucleotide-gated (HCN) channel isoforms and microRNA (miRNA-1 and miR-133) expression were evaluated by reverse transcription quantitative PCR. KEY

resultsMaximal specific conductance of I(f) was increased in MI, versus sham, in LV (P < 0.01) and LA myocytes (P < 0.05). Ivabradine reduced HR in both MI and sham rats (P < 0.05). In MI + IVA, I(f) overexpression was attenuated and HCN4 transcription reduced by 66% and 54% in LV and RV tissue, respectively, versus MI rats (all P < 0.05). miR-1 and miR-133, which modulate post-transcriptional expression of HCN2 and HCN4 genes, were significantly increased in myocytes from MI + IVA. CONCLUSION AND IMPLICATION: The beneficial effects of ivabradine may be due to the reversal of electrophysiological cardiac remodelling in post-MI rats by reduction of functional overexpression of HCN channels. This is attributable to transcriptional and post-transcriptional mechanisms.

Indexed as

AnimalsBenzazepinesCyclic Nucleotide-Gated Cation ChannelsHeart AtriaHeart RateHeart VentriclesHyperpolarization-Activated Cyclic Nucleotide-Gated ChannelsIon ChannelsIvabradineMaleMicroRNAsMyocardial InfarctionMyocytes, CardiacPotassium ChannelsRatsRats, WistarBenzazepinesCyclic Nucleotide-Gated Cation ChannelsHcn2 protein, ratHCN4 protein, ratHyperpolarization-Activated Cyclic Nucleotide-Gated ChannelsIon ChannelsIvabradineMicroRNAsMIRN133 microRNA, ratMIRN1 microRNA, ratPotassium Channels

Identifiers

PMID21838751
PMCPMC3372729
OpenAlexW1884338871

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.