ArticlePloS one2017
TGFBI functions similar to periostin but is uniquely dispensable during cardiac injury.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 53 citations in OpenAlex.
- Serum periostin levels in myocardial infarction: Findings from forensic autopsy cases.PloS one · 2026Article
- Cardioprotective Peptides from Dry-Cured Ham in Primary Endothelial Cells and Human Plasma: An Omics Approach.Antioxidants (Basel, Switzerland) · 2025Article
- Endurance Training Provokes Arrhythmogenic Right Ventricular Cardiomyopathy Phenotype in Heterozygous Desmoglein-2 Mutants: Alleviation by Preload Reduction.Biomedicines · 2024Article
- Impaired Relaxation in Induced Pluripotent Stem Cell-Derived Cardiomyocytes with PathogenicJournal of the American Heart Association · 2024Article
- Enter the Matrix: Fibroblast-immune cell interactions shape extracellular matrix deposition in health and disease.F1000Research · 2024Review
- Proteomics study and protein biomarkers of malignant ventricular arrhythmia in acute myocardial infarction patients.Clinical and translational medicine · 2023Article
- Pathogenic Roles of Cardiac Fibroblasts in Pediatric Dilated Cardiomyopathy.Journal of the American Heart Association · 2023Article
- Proteomic Analysis of Dupuytren's Contracture-Derived Sweat Glands Revealed the Synthesis of Connective Tissue Growth Factor and Initiation of Epithelial-Mesenchymal Transition as Major Pathogenetic Events.International journal of molecular sciences · 2023Article
- Defining the timeline of periostin upregulation in cardiac fibrosis following acute myocardial infarction in mice.Scientific reports · 2022Article
- Identification of Hub Genes in the Remodeling of Non-Infarcted Myocardium Following Acute Myocardial Infarction.Journal of cardiovascular development and disease · 2022Article
- Proteomic analysis identifies a signature of disease severity in the plasma of COVID-19 pneumonia patients associated to neutrophil, platelet and complement activation.Clinical proteomics · 2022Article
- Tissue mechanics coevolves with fibrillar matrisomes in healthy and fibrotic tissues.Matrix biology : journal of the International Society for Matrix Biology · 2022Review
- Dissecting the cellular landscape and transcriptome network in viral myocarditis by single-cell RNA sequencing.iScience · 2022Article
- Identification of the Potential Molecular Mechanism ofComputational and mathematical methods in medicine · 2022Article
- Functions of Matricellular Proteins in Dental Tissues and Their Emerging Roles in Orofacial Tissue Development, Maintenance, and Disease.International journal of molecular sciences · 2021Review
- Interleukin-1α dependent survival of cardiac fibroblasts is associated with StAR/STARD1 expression and improved cardiac remodeling and function after myocardial infarction.Journal of molecular and cellular cardiology · 2021Article
- Integrated bioinformatics analysis reveals novel key biomarkers and potential candidate small molecule drugs in gestational diabetes mellitus.Bioscience reports · 2021Article
- Endothelial angiogenic activity and adipose angiogenesis is controlled by extracellular matrix protein TGFBI.Scientific reports · 2021Article
- Transforming Growth Factor-induced Protein Promotes NF-κB-mediated Angiogenesis during Postnatal Lung Development.American journal of respiratory cell and molecular biology · 2021Article
- Periostin and matrix stiffness combine to regulate myofibroblast differentiation and fibronectin synthesis during palatal healing.Matrix biology : journal of the International Society for Matrix Biology · 2020Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Extracellular matrix production and accumulation stabilize the heart under normal conditions as well as form a protective scar after myocardial infarction injury, although excessive extracellular matrix accumulation with long-standing heart disease is pathological. In the current study we investigate the role of the matricellular protein, transforming growth factor beta-induced (TGFBI), which is induced in various forms of heart disease. Additionally, we sought to understand whether TGFBI is functionally redundant to its closely related family member periostin, which is also induced in the diseased heart. Surgical models of myocardial infarction and cardiac pressure overload were used in mice with genetic loss of Postn and/or Tgfbi to examine the roles of these genes during the fibrotic response. Additionally, cardiac-specific TGFBI transgenic mice were generated and analyzed. We observed that deletion of Tgfbi did not alter cardiac disease after myocardial infarction in contrast to greater ventricular wall rupture in Postn gene-deleted mice. Moreover, Tgfbi and Postn double gene-deleted mice showed a similar post-myocardial infarction disease phenotype as Postn-deleted mice. Over-expression of TGFBI in the hearts of mice had a similar effect as previously shown in mice with periostin over-expression. Thus, TGFBI and periostin act similarly in the heart in affecting fibrosis and disease responsiveness, although TGFBI is not seemingly necessary in the heart after myocardial infarction injury and is fully compensated by the more prominently expressed effector periostin.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.