Evidence map›Paper›PMID 21409385›Full record

ReviewPflugers Archiv : European journal of physiology2011

Impact of myocyte strain on cardiac myofilament activation.

Kenneth S Campbell

Abstract readReview
In one paragraph

Review in Pflugers Archiv : European journal of physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
–field-weighted citation impact
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

28 citing papers in PubMed.

  1. Myosin-actin crossbridge independent sarcomere length induced CaJournal of molecular and cellular cardiology · 2025
    Article
  2. CaJournal of molecular and cellular cardiology · 2025
    Article
  3. Multiscale modeling shows how 2'-deoxy-ATP rescues ventricular function in heart failure.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Sarcomere length-dependent effects on CaThe Journal of general physiology · 2019
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Mechanobiology in cardiac physiology and diseases.Journal of cellular and molecular medicine · 2013
    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

1 author.

Kenneth S CampbellDepartment of Physiology and Center for Muscle Biology, University of Kentucky, Lexington, KY, USA. k.s.campbell@uky.edu

Funding

Kentucky Center for Clinical and Translational ScienceUL1TR001998 · NCATS · UNIVERSITY OF KENTUCKY · PI HARTMANN, KATHERINE E, KERN, PHILIP A · 2016 to 2025
$34.2M
Kentucky Center for Clinical and Translational ScienceUL1TR000117 · NCATS · UNIVERSITY OF KENTUCKY · PI KERN, PHILIP A · 2012 to 2015
$13.3M
Myocardial Stiffness in Diastolic Heart FailureR01HL090749 · NHLBI · UNIVERSITY OF KENTUCKY · PI CAMPBELL, KENNETH S · 2008 to 2012
$1.6M
NCATS NIH HHS UL1 TR000117NCATS NIH HHS UL1 TR001998NHLBI NIH HHS HL090749NHLBI NIH HHS R01 HL090749
6 · The paper itself

Abstract

When cardiac myocytes are stretched by a longitudinal strain, they develop proportionally more active force at a given sub-maximal Ca(2+) concentration than they did at the shorter length. This is known as length-dependent activation. It is one of the most important contributors to the Frank-Starling relationship, a critical part of normal cardiovascular function. Despite intense research efforts, the mechanistic basis of the Frank-Starling relationship remains unclear. Potential mechanisms involving myofibrillar lattice spacing, titin-based effects, and cooperative activation have all been proposed. This review summarizes some of these mechanisms and discusses two additional potential theories that reflect the effects of localized strains that occur within and between half-sarcomeres. The main conclusion is that the Frank-Starling relationship is probably the integrated result of many interacting molecular mechanisms. Multiscale computational modeling may therefore provide the best way of determining the key processes that underlie length-dependent activation and their relative strengths.

Indexed as

Actin CytoskeletonAnimalsCalciumConnectinMechanotransduction, CellularMuscle ProteinsMyocardial ContractionMyocytes, CardiacProtein KinasesSarcomeresStress, MechanicalCalciumConnectinMuscle ProteinsProtein Kinases

Identifiers

PMID21409385
PMCPMC3115504

What OpenQuestion 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 OpenQuestion graph.