ArticleJournal of the American Heart Association2020
Defining the Cardiac Fibroblast Secretome in a Fibrotic Microenvironment.
Article in Journal of the American Heart Association, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 54 citations in OpenAlex.
- The 3D World of Spheroids: Searching for an Optimal Method of Fabricating Pro-Reparative Cardiospheres.International journal of molecular sciences · 2025Article
- PTEN Regulates Myofibroblast Activation in Valvular Interstitial Cells Based on Subcellular Localization.Advanced biology · 2025Article
- A secretome atlas of cardiac fibroblasts from healthy and infarcted mouse hearts.Communications biology · 2025Article
- Persistent Fibrosis in Heart Failure With a Reduced Ejection Fraction Linked to Phenotypic Differences in Human Cardiac Fibroblast Populations.Journal of the American Heart Association · 2025Article
- Cardiac Fibroblasts: Helping or Hurting.Genes · 2025Review
- Secreted Cytokines From Inflammatory Macrophages Modulate Sex Differences in Valvular Interstitial Cells on Hydrogel Biomaterials.Journal of biomedical materials research. Part A · 2025Article
- Investigations of cardiac fibrosis rheology by in vitro cardiac tissue modeling with 3D cellular spheroids.Journal of the mechanical behavior of biomedical materials · 2024Article
- The local mechanosensitive response of primary cardiac fibroblasts is influenced by the microenvironment mechanics.Scientific reports · 2024Article
- Review
- Preventive and treatment efficiency of dendrosomal nano-curcumin against ISO-induced cardiac fibrosis in mouse model.PloS one · 2024Article
- Substrate stiffness modulates cardiac fibroblast activation, senescence, and proinflammatory secretory phenotype.American journal of physiology. Heart and circulatory physiology · 2024Article
- Novel Peritoneal Sclerosis Rat Model Developed by Administration of Bleomycin and Lansoprazole.International journal of molecular sciences · 2023Article
- Regulation of cardiac fibroblasts by lymphocytes after a myocardial infarction: playing in the major league.American journal of physiology. Heart and circulatory physiology · 2023Review
- Chronic activation of human cardiac fibroblasts in vitro attenuates the reversibility of the myofibroblast phenotype.Scientific reports · 2023Article
- Exploration of Mediators Associated with Myocardial Remodelling in Feline Hypertrophic Cardiomyopathy.Animals : an open access journal from MDPI · 2023Article
- Low expression of miR-1929-3p mediates murine cytomegalovirus-induced fibrosis in cardiac fibroblasts via targeting endothelin a receptor/NLRP3 inflammasome pathway.In vitro cellular & developmental biology. Animal · 2023Article
- Extracellular matrix stiffness controls cardiac valve myofibroblast activation through epigenetic remodeling.Bioengineering & translational medicine · 2022Article
- Piezo1 Channel as a Potential Target for Hindering Cardiac Fibrotic Remodeling.International journal of molecular sciences · 2022Review
- Article
- Nuclear mechanosensing drives chromatin remodelling in persistently activated fibroblasts.Nature biomedical engineering · 2021Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Background Cardiac fibroblasts (CFs) have the ability to sense stiffness changes and respond to biochemical cues to modulate their states as either quiescent or activated myofibroblasts. Given the potential for secretion of bioactive molecules to modulate the cardiac microenvironment, we sought to determine how the CF secretome changes with matrix stiffness and biochemical cues and how this affects cardiac myocytes via paracrine signaling. Methods and Results Myofibroblast activation was modulated in vitro by combining stiffness cues with TGFβ1 (transforming growth factor β 1) treatment using engineered poly (ethylene glycol) hydrogels, and in vivo with isoproterenol treatment. Stiffness, TGFβ1, and isoproterenol treatment increased AKT (protein kinase B) phosphorylation, indicating that this pathway may be central to myofibroblast activation regardless of the treatment. Although activation of AKT was shared, different activating cues had distinct effects on downstream cytokine secretion, indicating that not all activated myofibroblasts share the same secretome. To test the effect of cytokines present in the CF secretome on paracrine signaling, neonatal rat ventricular cardiomyocytes were treated with CF conditioned media. Conditioned media from myofibroblasts cultured on stiff substrates and activated by TGFβ1 caused hypertrophy, and one of the cytokines in that media was insulin growth factor 1, which is a known mediator of cardiac myocyte hypertrophy. Conclusions Culturing CFs on stiff substrates, treating with TGFβ1, and in vivo treatment with isoproterenol all caused myofibroblast activation. Each cue had distinct effects on the secretome or genes encoding the secretome, but only the secretome of activated myofibroblasts on stiff substrates treated with TGFβ1 caused myocyte hypertrophy, most likely through insulin growth factor 1.
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