ArticleBasic research in cardiology2012
Increased afterload induces pathological cardiac hypertrophy: a new in vitro model.
Article in Basic research in cardiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers.
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Who cites it
100 citing papers in PubMed, 150 citations in OpenAlex.
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- Forced intensity-controlled endurance training on a small-animal treadmill machine inducing murine cardiac hypertrophy: insights and comparison to voluntary running models.Frontiers in pharmacology · 2025Article
- Advancing 3D Engineered In Vitro Models for Heart Failure Research: Key Features and Considerations.Bioengineering (Basel, Switzerland) · 2024Review
- Progress of organoid platform in cardiovascular research.Bioactive materials · 2024Review
- Dynamic control of contractile resistance to iPSC-derived micro-heart muscle arrays.Journal of biomedical materials research. Part A · 2024Article
- Biomechanical Impact of Pathogenic MYBPC3 Truncation Variant Revealed by Dynamically Tuning In Vitro Afterload.Journal of cardiovascular translational research · 2023Article
- Harnessing developmental cues for cardiomyocyte production.Development (Cambridge, England) · 2023Review
- Dynamic mechanobiology of cardiac cells and tissues: Current status and future perspective.Biophysics reviews · 2023Review
- Cardiomyocyte Maturation-the Road is not Obstructed.Stem cell reviews and reports · 2022Review
- Myocardial Fatigue: a Mechano-energetic Concept in Heart Failure.Current cardiology reports · 2022Review
- Piezo2 is not an indispensable mechanosensor in murine cardiomyocytes.Scientific reports · 2022Article
- EGR1 Is Implicated in Right Ventricular Cardiac Remodeling Associated with Pulmonary Hypertension.Biology · 2022Article
- Engineering a living cardiac pump on a chip using high-precision fabrication.Science advances · 2022Article
- MicroRNA miR-27a-3p accelerates cardiac hypertrophy by targeting neuro-oncological ventral antigen 1.Bioengineered · 2022Article
40 more citing papers are in PubMed but not listed here.
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Authors and funding
13 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Increased afterload results in 'pathological' cardiac hypertrophy, the most important risk factor for the development of heart failure. Current in vitro models fall short in deciphering the mechanisms of hypertrophy induced by afterload enhancement. The aim of this study was to develop an experimental model that allows investigating the impact of afterload enhancement (AE) on work-performing heart muscles in vitro. Fibrin-based engineered heart tissue (EHT) was cast between two hollow elastic silicone posts in a 24-well cell culture format. After 2 weeks, the posts were reinforced with metal braces, which markedly increased afterload of the spontaneously beating EHTs. Serum-free, triiodothyronine-, and hydrocortisone-supplemented medium conditions were established to prevent undefined serum effects. Control EHTs were handled identically without reinforcement. Endothelin-1 (ET-1)- or phenylephrine (PE)-stimulated EHTs served as positive control for hypertrophy. Cardiomyocytes in EHTs enlarged by 28.4 % under AE and to a similar extent by ET-1- or PE-stimulation (40.6 or 23.6 %), as determined by dystrophin staining. Cardiomyocyte hypertrophy was accompanied by activation of the fetal gene program, increased glucose consumption, and increased mRNA levels and extracellular deposition of collagen-1. Importantly, afterload-enhanced EHTs exhibited reduced contractile force and impaired diastolic relaxation directly after release of the metal braces. These deleterious effects of afterload enhancement were preventable by endothelin-A, but not endothelin-B receptor blockade. Sustained afterload enhancement of EHTs alone is sufficient to induce pathological cardiac remodeling with reduced contractile function and increased glucose consumption. The model will be useful to investigate novel therapeutic approaches in a simple and fast manner.
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