Evidence map›Paper›PMID 25505419›Full record

ReviewFrontiers in physiology2014

Role of sinoatrial node architecture in maintaining a balanced source-sink relationship and synchronous cardiac pacemaking.

Sathya D Unudurthi, Roseanne M Wolf, Thomas J Hund

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
2.2field-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

39 citing papers in PubMed, 1 synthesis or guideline pooled it, 74 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Stress-induced pacemaker desynchronization in the sinoatrial node.Frontiers in cardiovascular medicine · 2026
    Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Cardiac PDGFRαFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023
    Article
  14. Sinus node dysfunction: current understanding and future directions.American journal of physiology. Heart and circulatory physiology · 2023
    Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Implementing Biological Pacemakers: Design Criteria for Successful.Circulation. Arrhythmia and electrophysiology · 2021
    Review
  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

3 authors at 2 institutions in 1 country.

Sathya D UnudurthiDepartment of Biomedical Engineering, College of Engineering, The Ohio State University Columbus, OH, USA ; The Dorothy M. Davis Heart and Lung Research Institute, The Ohio State University Wexner Medical Center Columbus, OH, USA.
Roseanne M WolfDepartment of Mathematics, The University of Dubuque Dubuque, IA, USA.
Thomas J HundDepartment of Biomedical Engineering, College of Engineering, The Ohio State University Columbus, OH, USA ; The Dorothy M. Davis Heart and Lung Research Institute, The Ohio State University Wexner Medical Center Columbus, OH, USA ; Division of Cardiovascular Medicine, Department of Internal Medicine, The Ohio State University Wexner Medical Center Columbus, OH, USA.
The Ohio State University · USUniversity of Dubuque · US

Funding

CaMKII-dependent regulation of cardiac excitabilityR01HL114893 · NHLBI · OHIO STATE UNIVERSITY · PI HUND, THOMAS JEFFREY · 2012 to 2016
$1.9M
NHLBI NIH HHS R01 HL114893
6 · The paper itself

Abstract

Normal heart rhythm (sinus rhythm) depends on regular activity of the sinoatrial node (SAN), a heterogeneous collection of specialized myocytes in the right atrium. SAN cells, in general, possess a unique electrophysiological profile that promotes spontaneous electrical activity (automaticity). However, while automaticity is required for normal pacemaking, it is not necessarily sufficient. Less appreciated is the importance of the elaborate structure of the SAN complex for proper pacemaker function. Here, we review the important structural features of the SAN with a focus on how these elements help manage a precarious balance between electrical charge generated by the SAN ("source") and the charge needed to excite the surrounding atrial tissue ("sink"). We also discuss how compromised "source-sink" balance due, for example to fibrosis, may promote SAN dysfunction, characterized by slow and/or asynchronous pacemaker activity and even failure, in the setting of cardiovascular disease (e.g., heart failure, atrial fibrillation). Finally, we discuss implications of the "source-sink" balance in the SAN complex for cell and gene therapies aimed at creating a biological pacemaker as replacement or bridge to conventional electronic pacemakers.

Indexed as

arrhythmiaautomaticityintercellular couplingpacemakingsick sinus syndromesinoatrial nodesource-sink relationship

Identifiers

PMID25505419
PMCPMC4244803
OpenAlexW2082352304

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.