Evidence map›Paper›PMID 17123098›Full record

ArticlePflugers Archiv : European journal of physiology2007

Tension generation and relaxation in single myofibrils from human atrial and ventricular myocardium.

Nicoletta Piroddi, Alexandra Belus, Beatrice Scellini, Chiara Tesi, Gabriele Giunti, Elisabetta Cerbai, Alessandro Mugelli, Corrado Poggesi

Abstract read
PubMed Publisher
In one paragraph

Article in Pflugers Archiv : European journal of physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

64 citing papers in PubMed, 86 citations in OpenAlex.

  1. Evidence for a role of adverse sarcomere signaling in atrial fibrillation induction.Journal of molecular and cellular cardiology plus · 2026
    Review
  2. Article
  3. Article
  4. Article
  5. KFrontiers in physiology · 2025
    Article
  6. Article
  7. Article
  8. Fine tuning contractility: atrial sarcomere function in health and disease.American journal of physiology. Heart and circulatory physiology · 2024
    Review
  9. Article
  10. Myosin-binding protein H-like regulates myosin-binding protein distribution and function in atrial cardiomyocytes.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Effect of Myosin Isoforms on Cardiac Muscle Twitch of Mice, Rats and Humans.International journal of molecular sciences · 2022
    Article
  18. Article
  19. Review
  20. Alpha and beta myosin isoforms and human atrial and ventricular contraction.Cellular and molecular life sciences : CMLS · 2021
    Review

4 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

Nicoletta PiroddiCentro Interuniversitario di Medicina Molecolare e Biofisica Applicata, Florence, Italy.
Alexandra Belus
Beatrice Scellini
Chiara Tesi
Gabriele Giunti
Elisabetta Cerbai
Alessandro Mugelli
Corrado Poggesi
University of Florence · ITAzienda Ospedaliero-Universitaria Careggi · IT

Funding

Telethon GGP02428
6 · The paper itself

Abstract

Fast solution switching techniques in single myofibrils offer the opportunity to dissect and directly examine the sarcomeric mechanisms responsible for force generation and relaxation. The feasibility of this approach is tested here in human cardiac myofibrils isolated from small samples of atrial and ventricular tissue. At sarcomere lengths between 2.0 and 2.3 mum, resting tensions were significantly higher in ventricular than in atrial myofibrils. The rate constant of active tension generation after maximal Ca(2+) activation (k (ACT)) was markedly faster in atrial than in ventricular myofibrils. In both myofibril types k (ACT) was the same as the rate of tension redevelopment after mechanical perturbations and decreased significantly by decreasing [Ca(2+)] in the activating solution. Upon sudden Ca(2+) removal, active tension fully relaxed. Relaxation kinetics were (1) much faster in atrial than in ventricular myofibrils, (2) unaffected by bepridil, a drug that increases the affinity of troponin for Ca(2+), and (3) strongly accelerated by small increases in inorganic phosphate concentration. The results indicate that myofibril tension activation and relaxation rates reflect apparent cross-bridge kinetics and their Ca(2+) regulation rather than the rates at which thin filaments are switched on or off by Ca(2+) binding or removal. Myofibrils from human hearts retain intact mechanisms for contraction regulation and tension generation and represent a viable experimental model to investigate function and dysfunction of human cardiac sarcomeres.

Indexed as

AdultAgedCalciumDose-Response Relationship, DrugFeasibility StudiesFemaleHeartHeart AtriaHeart VentriclesHumansKineticsMaleMiddle AgedMyocardial ContractionMyocardiumMyofibrilsCalciumPhosphatesSolutions

Identifiers

PMID17123098
OpenAlexW2061780089

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.