Evidence map›Paper›PMID 20213494›Full record

ReviewPflugers Archiv : European journal of physiology2010

HCN-related channelopathies.

Mirko Baruscotti, Georgia Bottelli, Raffaella Milanesi, Jacopo C DiFrancesco, Dario DiFrancesco

Abstract readReview
PubMed Publisher
In one paragraph

Review in Pflugers Archiv : European journal of physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 1 pooled it
5.7field-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

53 citing papers in PubMed, 1 synthesis or guideline pooled it, 98 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Review
  6. The W101CInternational journal of molecular sciences · 2023
    Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Channelopathies of voltage-gated L-type Cav1.3/αPflugers Archiv : European journal of physiology · 2020
    Review
  14. Cardiac and neuronal HCN channelopathies.Pflugers Archiv : European journal of physiology · 2020
    Review
  15. Inhibition of G protein-gated KScientific reports · 2020
    Article
  16. The missense variant p.(Gly482Arg) inHeartRhythm case reports · 2020
    Article
  17. Review
  18. Article
  19. Article
  20. 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

5 authors at 2 institutions in 1 country.

Mirko BaruscottiDepartment of Biomolecular Sciences and Biotechnology, The PaceLab, University of Milano and Centro Interuniversitario di Medicina Molecolare e Biofisica Applicata (CIMMBA), Milano, Italy. mirko.baruscotti@unimi.it
Georgia Bottelli
Raffaella Milanesi
Jacopo C DiFrancesco
Dario DiFrancesco
University of Milan · ITUniversity of Milano-Bicocca · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

HCN channels are the molecular subunits of native funny (f-) channels of cardiac pacemaker cells and neurons. Although funny channels were first functionally described in cardiac cells in the late 1970s, cloning of HCN channels, of which four subunits are known today (HCN1-4), had to wait some 20 years to be accomplished, which delayed the investigation of HCN-related channelopathies. In cardiac pacemaker cells, the main function of f-channels is to contribute substantially to the generation of spontaneous activity of pacemaker cells and control of heart rate. Given this role in cardiac rhythm, it is natural to expect that defective f-channels (or their molecular correlates HCN4 channels) might be responsible for inheritable forms of cardiac arrhythmogenic diseases. Indeed, the recent search for HCN4-related inheritable arrhythmias has resulted in the finding of four different mutations of the hHcn4 gene, which have been reported to be associated with bradycardia and/or more complex arrhythmic conditions. In neurons, HCN channels display a variety of functions including the regulation of excitability, dendritic integration, plasticity, motor learning, generation of repetitive firing, and others. Defective HCN channels may therefore in principle also contribute to pathological conditions in the nervous system. While full evidence for neuronal HCN channelopathies is not yet available, several indications point to a link between temporal lobe and absence epilepsies and altered distribution of HCN1/HCN2 isoforms. Here we briefly review the current knowledge of HCN-related channelopathies in the heart and the brain.

Indexed as

Amino Acid SequenceArrhythmias, CardiacChannelopathiesCyclic Nucleotide-Gated Cation ChannelsEpilepsyHeartHumansHyperpolarization-Activated Cyclic Nucleotide-Gated ChannelsIon Channel GatingMolecular Sequence DataMuscle ProteinsPotassium ChannelsProtein IsoformsSinoatrial NodeCyclic Nucleotide-Gated Cation ChannelsHCN1 protein, humanHCN4 protein, humanHyperpolarization-Activated Cyclic Nucleotide-Gated ChannelsMuscle ProteinsPotassium ChannelsProtein Isoforms

Identifiers

PMID20213494
OpenAlexW1983786684

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.