ArticleThe Journal of pathology2012
Chronic cardiac allograft rejection: critical role of ED-A(+) fibronectin and implications for targeted therapy strategies.
Article in The Journal of pathology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- Certain role of extra-domain A containing fibronectin in the development of pulmonary hypertension in the sugen/hypoxia mouse model.Cardiovascular diagnosis and therapy · 2026Article
- A stage-based framework to interpret regulatory T cell biology after heart transplantation.Frontiers in cardiovascular medicine · 2026Review
- Computational pathology assessments of cardiac stromal remodeling: Clinical correlates and prognostic implications in heart transplantation.JHLT open · 2025Article
- Computational Pathology Assessments of Cardiac Stromal Remodeling: Clinical Correlates and Prognostic Implications in Heart Transplantation.Research square · 2024Article
- Serum Liberation of Fetal Fibronectin Variants in Patients with Pulmonary Hypertension: ED-AJournal of clinical medicine · 2021Article
- Allograft or Recipient ST2 Deficiency Oppositely Affected Cardiac Allograft VasculopathyFrontiers in immunology · 2021Article
- Serum Biomarkers of Cardiovascular Remodelling Reflect Extra-Valvular Cardiac Damage in Patients with Severe Aortic Stenosis.International journal of molecular sciences · 2020Article
- Assessment of Circulating Protein Signatures for Kidney Transplantation in Pediatric Recipients.Frontiers in medicine · 2017Article
- Article
- Detection of Soluble ED-A(+) Fibronectin and Evaluation as Novel Serum Biomarker for Cardiac Tissue Remodeling.Disease markers · 2016Article
- De novo expression of fetal ED-A(+) fibronectin and B (+) tenascin-C splicing variants in human cardiac allografts: potential impact for targeted therapy of rejection.Journal of molecular histology · 2014Article
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic cardiac allograft rejection is characterized by cardiac allograft vasculopathy (CAV) and cardiac interstitial fibrosis (CIF) causing severe long-term complications after heart transplantation and determining allograft function and patients' prognosis. Until now, there have been no sufficient preventive or therapeutic strategies. CAV and CIF are accompanied by changes in the extracellular matrix, including re-expression of the fetal fibronectin splice variant known as ED-A(+) fibronectin. This molecule has been shown to be crucial for the development of myofibroblasts (MyoFbs) as the main cell type in CIF and for the activation of vascular smooth muscle cells (VSMCs) as the main cell type in CAV. Relevant re-expression and protein deposition of ED-A(+) fibronectin has been demonstrated in animal models of chronic rejection, with spatial association to CAV and CIF, and a quantitative correlation to the rejection grade. The paper by Booth et al published in this issue of The Journal of Pathology could prove for the first time the functional importance of ED-A(+) fibronectin for the development of CIF as a main component of chronic cardiac rejection. Thus, promising conclusions for the development of new diagnostic, preventive, and therapeutic strategies for chronic cardiac rejection focusing on ED-A(+) fibronectin can be suggested.
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