ArticleBiochemistry research international2012
Length and PKA Dependence of Force Generation and Loaded Shortening in Porcine Cardiac Myocytes.
Article in Biochemistry research international, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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.
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
16 citing papers in PubMed, 20 citations in OpenAlex.
- Thin filament regulation of cardiac muscle power output: Implications for targets to improve human failing hearts.The Journal of general physiology · 2023Article
- Development and prevention of ischemic contracture ("stone heart") in the pig heart.Frontiers in cardiovascular medicine · 2023Article
- Mechano-calcium and mechano-electric feedbacks in the human cardiomyocyte analyzed in a mathematical model.The journal of physiological sciences : JPS · 2020Article
- Advanced Methodology and Preliminary Measurements of Molecular and Mechanical Properties of Heart Valves under Dynamic Strain.International journal of molecular sciences · 2020Article
- Regulation of Myofilament Contractile Function in Human Donor and Failing Hearts.Frontiers in physiology · 2020Article
- Chronic low-intensity exercise attenuates cardiomyocyte contractile dysfunction and impaired adrenergic responsiveness in aortic-banded mini-swine.Journal of applied physiology (Bethesda, Md. : 1985) · 2018Article
- Molecule specific effects of PKA-mediated phosphorylation on rat isolated heart and cardiac myofibrillar function.Archives of biochemistry and biophysics · 2016Article
- Saxagliptin and Tadalafil Differentially Alter Cyclic Guanosine Monophosphate (cGMP) Signaling and Left Ventricular Function in Aortic-Banded Mini-Swine.Journal of the American Heart Association · 2016Article
- The contributions of cardiac myosin binding protein C and troponin I phosphorylation to β-adrenergic enhancement of in vivo cardiac function.The Journal of physiology · 2016Article
- Elevated Ca2+ transients and increased myofibrillar power generation cause cardiac hypercontractility in a model of Noonan syndrome with multiple lentigines.American journal of physiology. Heart and circulatory physiology · 2015Article
- The contribution of cardiac myosin binding protein-c Ser282 phosphorylation to the rate of force generation and in vivo cardiac contractility.The Journal of physiology · 2014Article
- Titin-mediated control of cardiac myofibrillar function.Archives of biochemistry and biophysics · 2014Article
- A new twist on an old idea part 2: cyclosporine preserves normal mitochondrial but not cardiomyocyte function in mini-swine with compensated heart failure.Physiological reports · 2014Article
- Hypothesis and theory: mechanical instabilities and non-uniformities in hereditary sarcomere myopathies.Frontiers in physiology · 2014Article
- Length dependence of striated muscle force generation is controlled by phosphorylation of cTnI at serines 23/24.The Journal of physiology · 2013Article
- Calcium sensitivity and myofilament lattice structure in titin N2B KO mice.Archives of biochemistry and biophysics · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
In healthy hearts, ventricular ejection is determined by three myofibrillar properties; force, force development rate, and rate of loaded shortening (i.e., power). The sarcomere length and PKA dependence of these mechanical properties were measured in porcine cardiac myocytes. Permeabilized myocytes were prepared from left ventricular free walls and myocyte preparations were calcium activated to yield ~50% maximal force after which isometric force was measured at varied sarcomere lengths. Porcine myocyte preparations exhibited two populations of length-tension relationships, one being shallower than the other. Moreover, myocytes with shallow length-tension relationships displayed steeper relationships following PKA. Sarcomere length-K(tr) relationships also were measured and K(tr) remained nearly constant over ~2.30 μm to ~1.90 μm and then increased at lengths below 1.90 μm. Loaded-shortening and peak-normalized power output was similar at ~2.30 μm and ~1.90 μm even during activations with the same [Ca(2+)], implicating a myofibrillar mechanism that sustains myocyte power at lower preloads. PKA increased myocyte power and yielded greater shortening-induced cooperative deactivation in myocytes, which likely provides a myofibrillar mechanism to assist ventricular relaxation. Overall, the bimodal distribution of myocyte length-tension relationships and the PKA-mediated changes in myocyte length-tension and power are likely important modulators of Frank-Starling relationships in mammalian hearts.
Identifiers
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.