ArticleScientific reports2019
Biomechanical assessment of remote and postinfarction scar remodeling following myocardial infarction.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 28 citations in OpenAlex.
- Cardiac mechanotransduction from development to disease.APL bioengineering · 2026Review
- A prediction model for the risk of developing HFpEF during hospitalization in patients with acute myocardial infarction.International journal of cardiology. Heart & vasculature · 2026Article
- Article
- Human iPSC cardiomyocyte patch transplantation modifies extracellular matrix and fibroblast behavior after myocardial infarction.iScience · 2026Article
- Adamts1 Exacerbates Post-Myocardial Infarction Scar Formation via Mechanosensing of Integrin α8.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Chrysin Attenuates Myocardial Cell Apoptosis in Mice.Cardiovascular toxicology · 2025Article
- Plasmapheresis as a Potential Generalizable Therapy for Myocardial Infarction.Rejuvenation research · 2025Review
- Vitamin C in Cardiovascular Disease: From Molecular Mechanisms to Clinical Evidence and Therapeutic Applications.Antioxidants (Basel, Switzerland) · 2025Review
- Microparticle Mediated Delivery of Apelin Improves Heart Function in Post Myocardial Infarction Mice.Circulation research · 2024Article
- Mitigation of Fibrosis after Myocardial Infarction in Rats by Using a Porcine Cholecyst Extracellular Matrix.Comparative medicine · 2023Article
- Lack of expression of miR-29a/b1 impairs bladder function in male mice.Disease models & mechanisms · 2023Article
- Vitamin C Regulates the Profibrotic Activity of Fibroblasts in In Vitro Replica Settings of Myocardial Infarction.International journal of molecular sciences · 2023Article
- Ultrasonic Microbubble Cavitation Deliver Gal-3 shRNA to Inhibit Myocardial Fibrosis after Myocardial Infarction.Pharmaceutics · 2023Article
- Tropoelastin Improves Post-Infarct Cardiac Function.Circulation research · 2023Article
- Endogenous Modulation of Extracellular Matrix Collagen during Scar Formation after Myocardial Infarction.International journal of molecular sciences · 2022Article
- Fourier analysis of collagen bundle orientation in myocardial infarction scars.Histochemistry and cell biology · 2022Article
- Aminoacylase-1 plays a key role in myocardial fibrosis and the therapeutic effects of 20(S)-ginsenoside Rg3 in mouse heart failure.Acta pharmacologica Sinica · 2022Article
- Revealing the nanometric structural changes in myocardial infarction models by time-lapse intravital imaging.Frontiers in bioengineering and biotechnology · 2022Article
- Hopes and Hurdles of Employing Mesenchymal Stromal Cells in the Treatment of Cardiac Fibrosis.International journal of molecular sciences · 2021Review
- Engineering the Cellular Microenvironment of Post-infarct Myocardium on a Chip.Frontiers in cardiovascular medicine · 2021Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The importance of collagen remodeling following myocardial infarction (MI) is extensively investigated, but little is known on the biomechanical impact of fibrillar collagen on left ventricle post-MI. We aim to identify the significant effects of the biomechanics of types I, III, and V collagen on physio-pathological changes of murine hearts leading to heart failure. Immediately post-MI, heart reduces its function (EF = 40.94 ± 2.12%) while sarcomeres' dimensions are unchanged. Strikingly, as determined by immunohistochemistry staining, type V collagen fraction significantly grows in remote and scar for sustaining de novo-types I and III collagen fibers' assembly while hindering their enzymatic degradation. Thereafter, the compensatory heart function (EF = 63.04 ± 3.16%) associates with steady development of types I and III collagen in a stiff remote (12.79 ± 1.09 MPa) and scar (22.40 ± 1.08 MPa). In remote, the soft de novo-type III collagen uncoils preventing further expansion of elongated sarcomeres (2.7 ± 0.3 mm). Once the compensatory mechanisms are surpassed, the increased turnover of stiff type I collagen (>50%) lead to a pseudo-stable biomechanical regime of the heart (≅9 MPa) with reduced EF (50.55 ± 3.25%). These end-characteristics represent the common scenario evidenced in patients suffering from heart failure after MI. Our pre-clinical data advances the understanding of the cause of heart failure induced in patients with extended MI.
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