Evidence map›Paper›PMID 33383853›Full record

ReviewInternational journal of molecular sciences2020

Cardiac Connexin-43 Hemichannels and Pannexin1 Channels: Provocative Antiarrhythmic Targets.

Katarina Andelova, Tamara Egan Benova, Barbara Szeiffova Bacova, Matus Sykora, Natalia Jorgelina Prado, Emiliano Raul Diez, Peter Hlivak, Narcis Tribulova

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.7field-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

37 citing papers in PubMed, 50 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Modulation of Redox-Sensitive Cardiac Ion Channels.Antioxidants (Basel, Switzerland) · 2025
    Review
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  8. Review
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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

8 authors at 3 institutions in 2 countries.

Katarina AndelovaCentre of Experimental Medicine, Slovak Academy of Sciences, Institute for Heart Research, 84104 Bratislava, Slovakia.ORCID 0000-0002-1499-7687
Tamara Egan BenovaCentre of Experimental Medicine, Slovak Academy of Sciences, Institute for Heart Research, 84104 Bratislava, Slovakia.
Barbara Szeiffova BacovaCentre of Experimental Medicine, Slovak Academy of Sciences, Institute for Heart Research, 84104 Bratislava, Slovakia.ORCID 0000-0001-8394-7459
Matus SykoraCentre of Experimental Medicine, Slovak Academy of Sciences, Institute for Heart Research, 84104 Bratislava, Slovakia.ORCID 0000-0002-0438-3956
Natalia Jorgelina PradoInstituto de Medicina y Biología Experimental de Cuyo, Consejo Nacional de Investigaciones Científicas y Técnicas, M5500 Mendoza, Argentina.
Emiliano Raul DiezInstituto de Medicina y Biología Experimental de Cuyo, Consejo Nacional de Investigaciones Científicas y Técnicas, M5500 Mendoza, Argentina.ORCID 0000-0001-5163-3703
Peter HlivakDepartment of Arrhythmias and Pacing, National Institute of Cardiovascular Diseases, Pod Krásnou Hôrkou 1, 83348 Bratislava, Slovakia.
Narcis TribulovaCentre of Experimental Medicine, Slovak Academy of Sciences, Institute for Heart Research, 84104 Bratislava, Slovakia.ORCID 0000-0002-5904-4249
Slovak Academy of Sciences · SKConsejo Nacional de Investigaciones Científicas y Técnicas · ARNational Institute of Cardiovascular Diseases · SK

Funding

APVV 18-0548, 15-0376EU ITMS 26230120009Vedecká Grantová Agentúra MŠVVaŠ SR a SAV 2/0002/20, 2/0158/19
6 · The paper itself

Abstract

Cardiac connexin-43 (Cx43) creates gap junction channels (GJCs) at intercellular contacts and hemi-channels (HCs) at the peri-junctional plasma membrane and sarcolemmal caveolae/rafts compartments. GJCs are fundamental for the direct cardiac cell-to-cell transmission of electrical and molecular signals which ensures synchronous myocardial contraction. The HCs and structurally similar pannexin1 (Panx1) channels are active in stressful conditions. These channels are essential for paracrine and autocrine communication through the release of ions and signaling molecules to the extracellular environment, or for uptake from it. The HCs and Panx1 channel-opening profoundly affects intracellular ionic homeostasis and redox status and facilitates via purinergic signaling pro-inflammatory and pro-fibrotic processes. These conditions promote cardiac arrhythmogenesis due to the impairment of the GJCs and selective ion channel function. Crosstalk between GJCs and HCs/Panx1 channels could be crucial in the development of arrhythmogenic substrates, including fibrosis. Despite the knowledge gap in the regulation of these channels, current evidence indicates that HCs and Panx1 channel activation can enhance the risk of cardiac arrhythmias. It is extremely challenging to target HCs and Panx1 channels by inhibitory agents to hamper development of cardiac rhythm disorders. Progress in this field may contribute to novel therapeutic approaches for patients prone to develop atrial or ventricular fibrillation.

Indexed as

Ion Channel GatingAnimalsAnti-Arrhythmia AgentsArrhythmias, CardiacConnexin 43ConnexinsDisease SusceptibilityHumansMitochondria, HeartMyocardiumAnti-Arrhythmia AgentsConnexin 43Connexinscardiac arrhythmiascardio-protectionCx43 hemi-channelsmimetic peptidespannexin1 channels

Identifiers

PMID33383853
PMCPMC7795512
OpenAlexW3117353167

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.