Evidence map›Paper›PMID 33017571›Full record

ReviewAnnual review of pharmacology and toxicology2021

Pharmacologic Approach to Sinoatrial Node Dysfunction.

Pietro Mesirca, Vadim V Fedorov, Thomas J Hund, Angelo G Torrente, Isabelle Bidaud, Peter J Mohler, Matteo E Mangoni

Open access · bronzeAbstract readReview
In one paragraph

Review in Annual review of pharmacology and toxicology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
4.3field-weighted citation impact, top 4% 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

29 citing papers in PubMed, 46 citations in OpenAlex.

  1. Trial
  2. Emerging Regulatory Mechanisms in Sinoatrial Node Automaticity.Journal of cellular and molecular medicine · 2026
    Review
  3. Article
  4. Aging and sinus node dysfunction: mechanisms and future directions.Clinical science (London, England : 1979) · 2025
    Review
  5. Review
  6. Article
  7. Opto-chemogenetic inhibition of L-type CaCell reports methods · 2024
    Article
  8. Review
  9. Review
  10. Lipopolysaccharide-induced sepsis impairs M2R-GIRK signaling in the mouse sinoatrial node.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  11. Review
  12. Review
  13. Article
  14. Sinus node dysfunction: current understanding and future directions.American journal of physiology. Heart and circulatory physiology · 2023
    Review
  15. Pathophysiology of CaFrontiers in physiology · 2023
    Review
  16. Review
  17. Paradigm shift: new concepts for HCN4 function in cardiac pacemaking.Pflugers Archiv : European journal of physiology · 2022
    Review
  18. Article
  19. Review
  20. ESC working group on cardiac cellular electrophysiology position paper: relevance, opportunities, and limitations of experimental models for cardiac electrophysiology research.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2021
    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

7 authors at 6 institutions in 2 countries.

Pietro MesircaInstitut de Génomique Fonctionnelle, Université de Montpellier, CNRS, INSERM, 34096 Montpellier, France; email: matteo.mangoni@igf.cnrs.fr.
Vadim V FedorovFrick Center for Heart Failure and Arrhythmia at the Davis Heart and Lung Research Institute, The Ohio State University, Columbus, Ohio 43210, USA.
Thomas J HundFrick Center for Heart Failure and Arrhythmia at the Davis Heart and Lung Research Institute, The Ohio State University, Columbus, Ohio 43210, USA.
Angelo G TorrenteInstitut de Génomique Fonctionnelle, Université de Montpellier, CNRS, INSERM, 34096 Montpellier, France; email: matteo.mangoni@igf.cnrs.fr.
Isabelle BidaudInstitut de Génomique Fonctionnelle, Université de Montpellier, CNRS, INSERM, 34096 Montpellier, France; email: matteo.mangoni@igf.cnrs.fr.
Peter J MohlerFrick Center for Heart Failure and Arrhythmia at the Davis Heart and Lung Research Institute, The Ohio State University, Columbus, Ohio 43210, USA.
Matteo E MangoniInstitut de Génomique Fonctionnelle, Université de Montpellier, CNRS, INSERM, 34096 Montpellier, France; email: matteo.mangoni@igf.cnrs.fr.
The Ohio State University · USCentre National de la Recherche Scientifique · FRInserm · FRLaboratoire d'Excellence Canaux Ioniques d'Intérêt Thérapeutique · FRThe Ohio State University Wexner Medical Center · USUniversité de Montpellier · FR

Funding

Defining novel mechanisms for human arrhythmiaR35HL135754 · NHLBI · OHIO STATE UNIVERSITY · PI MOHLER, PETER J. · 2017 to 2023
$6.0M
Targeting the Arrhythmogenic Sources of Human Atrial FibrillationR01HL135109 · NHLBI · OHIO STATE UNIVERSITY · PI Vadim V Fedorov · 2017 to 2026
$6.0M
Integration of structure and signaling in cardiac pacemaker functionR01HL115580 · NHLBI · OHIO STATE UNIVERSITY · PI FEDOROV, VADIM V · 2013 to 2021
$4.2M
Defining novel mechanisms for regulation of atrial INa and arrhythmiasR01HL134824 · NHLBI · OHIO STATE UNIVERSITY · PI HUND, THOMAS JEFFREY, MOHLER, PETER J. · 2017 to 2020
$3.0M
Spectrin-based regulation of cardiac remodeling and heart failureR01HL135096 · NHLBI · OHIO STATE UNIVERSITY · PI HUND, THOMAS JEFFREY · 2017 to 2020
$1.6M
NHLBI NIH HHS R01 HL115580NHLBI NIH HHS R01 HL134824NHLBI NIH HHS R01 HL135096NHLBI NIH HHS R01 HL135109NHLBI NIH HHS R35 HL135754
6 · The paper itself

Abstract

The spontaneous activity of the sinoatrial node initiates the heartbeat. Sino-atrial node dysfunction (SND) and sick sinoatrial (sick sinus) syndrome are caused by the heart's inability to generate a normal sinoatrial node action potential. In clinical practice, SND is generally considered an age-related pathology, secondary to degenerative fibrosis of the heart pacemaker tissue. However, other forms of SND exist, including idiopathic primary SND, which is genetic, and forms that are secondary to cardiovascular or systemic disease. The incidence of SND in the general population is expected to increase over the next half century, boosting the need to implant electronic pacemakers. During the last two decades, our knowledge of sino-atrial node physiology and of the pathophysiological mechanisms underlying SND has advanced considerably. This review summarizes the current knowledge about SND mechanisms and discusses the possibility of introducing new pharmacologic therapies for treating SND.

Indexed as

Sick Sinus SyndromeSinoatrial NodeHeart Conduction SystemHumansankyrin-BCav1.3G protein–activated K+ channelsSANsinoatrial node dysfunctiontertiapin-Q

Identifiers

PMID33017571
PMCPMC7790915
OpenAlexW3090272320

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.