ArticleAmerican journal of physiology. Heart and circulatory physiology2014
Myofilament dysfunction contributes to impaired myocardial contraction in the infarct border zone.
Article in American journal of physiology. Heart and circulatory physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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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.
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Who cites it
15 citing papers in PubMed, 23 citations in OpenAlex.
- Post-MI Remodeling Mechanics of Left Ventricle: Microstructure-Informed Models, Identifiability, and Uncertainty for Patient-Specific Prediction.Bioengineering (Basel, Switzerland) · 2026Review
- CaBiophysical journal · 2025Article
- Multiscale fiber remodeling in the infarcted left ventricle using a stress-based reorientation law.Acta biomaterialia · 2024Article
- Post-infarct evolution of ventricular and myocardial function.Biomechanics and modeling in mechanobiology · 2023Article
- Reduced cardiac muscle power with low ATP simulating heart failure.Biophysical journal · 2022Article
- Lingbao Huxin Pill Alleviates Apoptosis and Inflammation at Infarct Border Zone through SIRT1-Mediated FOXO1 and NF- κ B Pathways in Rat Model of Acute Myocardial Infarction.Chinese journal of integrative medicine · 2022Article
- Myocardial injection of a thermoresponsive hydrogel with reactive oxygen species scavenger properties improves border zone contractility.Journal of biomedical materials research. Part A · 2020Article
- Angiotensin Receptor Neprilysin Inhibitor Attenuates Myocardial Remodeling and Improves Infarct Perfusion in Experimental Heart Failure.Scientific reports · 2019Article
- Acellular Extracellular Matrix Bioscaffolds for Cardiac Repair and Regeneration.Frontiers in cell and developmental biology · 2019Review
- Effects of hydrogel injection on borderzone contractility post-myocardial infarction.Biomechanics and modeling in mechanobiology · 2018Article
- Short term doxycycline treatment induces sustained improvement in myocardial infarction border zone contractility.PloS one · 2018Article
- αAmerican journal of physiology. Heart and circulatory physiology · 2017Article
- Mathematical modeling of cardiac growth and remodeling.Wiley interdisciplinary reviews. Systems biology and medicine · 2016Review
- Moderate Ischemic Mitral Regurgitation After Posterolateral Myocardial Infarction in Sheep Alters Left Ventricular Shear but Not Normal Strain in the Infarct and Infarct Borderzone.The Annals of thoracic surgery · 2016Article
- A Novel Method for Quantifying Smooth Regional Variations in Myocardial Contractility Within an Infarcted Human Left Ventricle Based on Delay-Enhanced Magnetic Resonance Imaging.Journal of biomechanical engineering · 2015Article
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
After myocardial infarction, a poorly contracting nonischemic border zone forms adjacent to the infarct. The cause of border zone dysfunction is unclear. The goal of this study was to determine the myofilament mechanisms involved in postinfarction border zone dysfunction. Two weeks after anteroapical infarction of sheep hearts, we studied in vitro isometric and isotonic contractions of demembranated myocardium from the infarct border zone and a zone remote from the infarct. Maximal force development (Fmax) of the border zone myocardium was reduced by 31 ± 2% versus the remote zone myocardium (n = 6/group, P < 0.0001). Decreased border zone Fmax was not due to a reduced content of contractile material, as assessed histologically, and from myosin content. Furthermore, decreased border zone Fmax did not involve altered cross-bridge kinetics, as assessed by muscle shortening velocity and force development kinetics. Decreased border zone Fmax was associated with decreased cross-bridge formation, as assessed from muscle stiffness in the absence of ATP where cross-bridge formation should be maximized (rigor stiffness was reduced 34 ± 6%, n = 5, P = 0.011 vs. the remote zone). Furthermore, the border zone myocardium had significantly reduced phosphorylation of myosin essential light chain (ELC; 41 ± 10%, n = 4, P < 0.05). However, for animals treated with doxycycline, an inhibitor of matrix metalloproteinases, rigor stiffness and ELC phosphorylation were not reduced in the border zone myocardium, suggesting that doxycycline had a protective effect. In conclusion, myofilament dysfunction contributes to postinfarction border zone dysfunction, myofilament dysfunction involves impaired cross-bridge formation and decreased ELC phosphorylation, and matrix metalloproteinase inhibition may be beneficial for limiting postinfarct border zone dysfunction.
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