ArticleAmerican journal of physiology. Heart and circulatory physiology2013
Mechanical and energetic properties of papillary muscle from ACTC E99K transgenic mouse models of hypertrophic cardiomyopathy.
Article in American journal of physiology. Heart and circulatory physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 28 citations in OpenAlex.
- A Cautionary Tale of Hypertrophic Cardiomyopathy-From "Benign" Left Ventricular Hypertrophy to Stroke, Atrial Fibrillation, and Molecular Genetic Diagnostics: A Case Report and Review of Literature.International journal of molecular sciences · 2024Review
- Strength training improves heart function, collagen and strength in rats with heart failure.The journal of physiological sciences : JPS · 2024Article
- Article
- Contractility detection of isolated mouse papillary muscle using myotronic Myostation-Intact device.Animal models and experimental medicine · 2022Article
- Critical Evaluation of Current Hypotheses for the Pathogenesis of Hypertrophic Cardiomyopathy.International journal of molecular sciences · 2022Review
- Force Measurements From Myofibril to Filament.Frontiers in physiology · 2021Review
- Isogenic models of hypertrophic cardiomyopathy unveil differential phenotypes and mechanism-driven therapeutics.Journal of molecular and cellular cardiology · 2020Article
- Large Animal Models in Regenerative Medicine and Tissue Engineering: To Do or Not to Do.Frontiers in bioengineering and biotechnology · 2020Review
- New insights provided by myofibril mechanics in inherited cardiomyopathies.Conditioning medicine · 2019Article
- Isogenic Pairs of hiPSC-CMs with Hypertrophic Cardiomyopathy/LVNC-Associated ACTC1 E99K Mutation Unveil Differential Functional Deficits.Stem cell reports · 2018Article
- Phenotyping cardiomyopathy in adult zebrafish.Progress in biophysics and molecular biology · 2018Review
- The Molecular Mechanisms of Mutations in Actin and Myosin that Cause Inherited Myopathy.International journal of molecular sciences · 2018Review
- Classifying Cardiac Actin Mutations Associated With Hypertrophic Cardiomyopathy.Frontiers in physiology · 2018Review
- Development of apical hypertrophic cardiomyopathy with age in a transgenic mouse model carrying the cardiac actin E99K mutation.Journal of muscle research and cell motility · 2017Article
- Age- and strain-related aberrant CaAmerican journal of physiology. Heart and circulatory physiology · 2017Article
- Investigations into the Sarcomeric Protein and CaFrontiers in physiology · 2017Article
- Phosphorylation of the regulatory light chain of myosin in striated muscle: methodological perspectives.European biophysics journal : EBJ · 2016Review
- Why Is there a Limit to the Changes in Myofilament CaFrontiers in physiology · 2016Review
- A dilated cardiomyopathy mutation blunts adrenergic response and induces contractile dysfunction under chronic angiotensin II stress.American journal of physiology. Heart and circulatory physiology · 2015Article
- The dilated cardiomyopathy-causing mutation ACTC E361G in cardiac muscle myofibrils specifically abolishes modulation of Ca(2+) regulation by phosphorylation of troponin I.Biophysical journal · 2014Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
We compared the contractile performance of papillary muscle from a mouse model of hypertrophic cardiomyopathy [α-cardiac actin (ACTC) E99K mutation] with nontransgenic (non-TG) littermates. In isometric twitches, ACTC E99K papillary muscle produced three to four times greater force than non-TG muscle under the same conditions independent of stimulation frequency and temperature, whereas maximum isometric force in myofibrils from these muscles was not significantly different. ACTC E99K muscle relaxed slower than non-TG muscle in both papillary muscle (1.4×) and myofibrils (1.7×), whereas the rate of force development after stimulation was the same as non-TG muscle for both electrical stimulation in intact muscle and after a Ca²⁺ jump in myofibrils. The EC₅₀ for Ca²⁺ activation of force in myofibrils was 0.39 ± 0.33 μmol/l in ACTC E99K myofibrils and 0.80 ± 0.11 μmol/l in non-TG myofibrils. There were no significant differences in the amplitude and time course of the Ca²⁺ transient in myocytes from ACTC E99K and non-TG mice. We conclude that hypercontractility is caused by higher myofibrillar Ca²⁺ sensitivity in ACTC E99K muscles. Measurement of the energy (work + heat) released in actively cycling heart muscle showed that for both genotypes, the amount of energy turnover increased with work done but with decreasing efficiency as energy turnover increased. Thus, ACTC E99K mouse heart muscle produced on average 3.3-fold more work than non-TG muscle, and the cost in terms of energy turnover was disproportionately higher than in non-TG muscles. Efficiency for ACTC E99K muscle was in the range of 11-16% and for non-TG muscle was 15-18%.
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