ArticleScientific reports2019
Myofibroblast modulation of cardiac myocyte structure and function.
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 32 papers.
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Who cites it
32 citing papers in PubMed, 57 citations in OpenAlex.
- Models of cardiomyocyte-non-myocyte electrical interactions.The Journal of physiology · 2026Review
- The mechanobiology of fibroblast activation in disease.APL bioengineering · 2025Review
- Tension-sensitive HOX gene expression in fibroblasts for differential scar formation.Journal of translational medicine · 2025Article
- The role of cardiac microenvironment in cardiovascular diseases: implications for therapy.Human cell · 2024Review
- Opto-SICM framework combines optogenetics with scanning ion conductance microscopy for probing cell-to-cell contacts.Communications biology · 2023Article
- Human myofibroblasts increase the arrhythmogenic potential of human induced pluripotent stem cell-derived cardiomyocytes.Cellular and molecular life sciences : CMLS · 2023Article
- Functional microvascularization of human myocardiumCell reports methods · 2022Article
- The caspase-1 inhibitor VX765 upregulates connexin 43 expression and improves cell-cell communication after myocardial infarction via suppressing the IL-1β/p38 MAPK pathway.Acta pharmacologica Sinica · 2022Article
- A strategy to quantify myofibroblast activation on a continuous spectrum.Scientific reports · 2022Article
- Single Nucleus RNA-sequencing Reveals Altered Intercellular Communication and Dendritic Cell Activation in Nonobstructive Hypertrophic Cardiomyopathy.Cardiology and cardiovascular medicine · 2022Article
- Scoping review and interpretation of myofascial pain/fibromyalgia syndrome: An attempt to assemble a medical puzzle.PloS one · 2022Article
- Effects of fibroblast on electromechanical dynamics of human atrial tissue-insights from a 2D discrete element model.Frontiers in physiology · 2022Article
- Pharmacological basis of the antifibrotic effects of pirfenidone: Mechanistic insights from cardiacFrontiers in cardiovascular medicine · 2022Review
- Article
- Micropattern platform promotes extracellular matrix remodeling by human PSC-derived cardiac fibroblasts and enhances contractility of co-cultured cardiomyocytes.Physiological reports · 2021Article
- Ventricular Arrhythmias in Ischemic Cardiomyopathy-New Avenues for Mechanism-Guided Treatment.Cells · 2021Review
- Review
- A new model of myofibroblast-cardiomyocyte interactions and their differences across species.Biophysical journal · 2021Article
- Mesenchymal Stem Cells Therapies on Fibrotic Heart Diseases.International journal of molecular sciences · 2021Review
- Diffuse myocardial fibrosis: mechanisms, diagnosis and therapeutic approaches.Nature reviews. Cardiology · 2021Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
After myocardial infarction, resident fibroblasts (Fb) differentiate towards myofibroblasts (MyoFb), generating the scar tissue and the interstitial fibrosis seen in the adjacent myocardium. Fb and MyoFb have the potential to interact with cardiac myocytes (CMs) but insight into the phenotype-specific role and mode of interaction is still incomplete. Our objectives are to further define the modulation of CMs by MyoFbs compared to Fbs, as well as the role of direct contact through gap junctions vs. soluble mediators, using Fbs and CMs from pig left ventricle. Fbs were treated to maintain an undifferentiated state (SD-208) or to attain full differentiation to MyoFb (TGF-β1). Fbs and MyoFbs were co-cultured with CMs, with the possibility of direct contact or separated by a Thincert membrane. Only in direct co-culture, both Fbs and MyoFbs were able to decrease CM viability after 2 days. Only MyoFbs induced significant distal spreading of CMs in both direct and indirect co-culture. MyoFbs, but not Fbs, readily made connections with CMs in direct co-culture and connexin 43 expression in MyoFb was higher than in Fb. When coupled to CMs, MyoFbs reduced the CM action potential duration and hyperpolarized the CM resting membrane potential. Uncoupling reversed these effects. In conclusion, MyoFbs, but not Fbs, alter the CM structural phenotype. MyoFbs, but not Fbs, are likely to electrically connect to CMs and thereby modulate the CM membrane potential. These data provide further support for an active role of MyoFbs in the arrhythmogenic substrate after cardiac remodelling.
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