ArticlePflugers Archiv : European journal of physiology2006
No direct effect of creatine phosphate on the cross-bridge cycle in cardiac myofibrils.
Article in Pflugers Archiv : European journal of physiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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.
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.
Who cites it
7 citing papers in PubMed, 18 citations in OpenAlex.
- Hypercontractility and Oxidative Stress Drive Creatine Kinase Dysfunction in Hypertrophic Cardiomyopathy.Circulation · 2025Article
- The effects of fatigue and oxidation on contractile function of intact muscle fibers and myofibrils isolated from the mouse diaphragm.Scientific reports · 2019Article
- A Novel Method of Isolating Myofibrils From Primary Cardiomyocyte Culture Suitable for Myofibril Mechanical Study.Frontiers in cardiovascular medicine · 2019Article
- The increase in non-cross-bridge forces after stretch of activated striated muscle is related to titin isoforms.American journal of physiology. Cell physiology · 2016Article
- Protein kinase A changes calcium sensitivity but not crossbridge kinetics in human cardiac myofibrils.American journal of physiology. Heart and circulatory physiology · 2011Article
- Calcium binding kinetics of troponin C strongly modulate cooperative activation and tension kinetics in cardiac muscle.Journal of molecular and cellular cardiology · 2011Article
- Sarcomere dynamics during muscular contraction and their implications to muscle function.Journal of muscle research and cell motility · 2007Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Creatine phosphate (CP) and creatine kinase (CK) are involved in the rapid resynthesis of ATP and thereby serve to stabilize ATP concentration and to maintain free ADP low inside cardiac muscle cells during contraction. Recently, it has been suggested from experiments in permeabilized multicellular preparations that CP/CK also regulate the kinetics of the actomyosin interaction (cross-bridge cycle) and may explain contractile dysfunction, for instance, during ischemia. However, the reported effects of CP/CK may be confounded by diffusion limitations in multicellular preparations in which inorganic phosphate (P(i)) and ADP may significantly accumulate during contraction. To test this hypothesis, we measured force production and the rates of force development (k (ACT) and k (TR)) in isolated cardiac myofibrils, in which rapid concentration changes of Ca(2+), CP/CK, and P(i) were imposed using a rapid perfusion change system. The results showed that CP/CK did not influence maximum force-generating capacity, whereas P(i) markedly reduced force and increased the rates of force development. No effects of CP/CK on the rates of force development were observed, consistent with the notion that CP/CK do not exert a direct effect on the actomyosin interaction.
Indexed as
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What OpenQuestion holds
Registered trials
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.