ArticleEuropean heart journal2013
Matricellular proteins and matrix metalloproteinases mark the inflammatory and fibrotic response in human cardiac allograft rejection.
Article in European heart journal, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 36 citations in OpenAlex.
- Fibrosis Process Activation in Patients with Acute Cardiac Rejection: A Novel Noninvasive Diagnostic Approach.Biomedicines · 2026Article
- Epigenetic regulation in transplant rejection and tolerance: mechanisms and therapeutic prospects.Frontiers in cardiovascular medicine · 2026Review
- The Role of Thrombospondin-2 in Myocardial Fibrosis.Drug design, development and therapy · 2026Review
- Prognostic Role of MMP2, MMP9, and IL-1β Markers in Cardiac Allograft Rejection After Transplantation.International journal of molecular sciences · 2025Article
- Cellular Rejection Post-Cardiac Transplantation: A 13-Year Single Unicentric Study.Medicina (Kaunas, Lithuania) · 2025Article
- Differential Effects of Brain Death and Circulatory Death on Myocardial Integrity and Transplant Outcomes.Journal of surgery and research · 2025Article
- Human leukocyte antigen class I antibody-activated endothelium promotes CD206+ M2 macrophage polarization and MMP9 secretion through TLR4 signaling and P-selectin in a model of antibody-mediated rejection and allograft vasculopathy.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2024Article
- Review
- Matrix Metalloproteinases and Heart Transplantation-A Pathophysiological and Clinical View.Medicina (Kaunas, Lithuania) · 2023Review
- Research Progress of Myocardial Fibrosis and Atrial Fibrillation.Frontiers in cardiovascular medicine · 2022Review
- Cardiac fibrosis.Cardiovascular research · 2021Review
- The Extracellular Matrix in Ischemic and Nonischemic Heart Failure.Circulation research · 2019Review
- Mineralocorticoid Receptor and Aldosterone-Related Biomarkers of End-Organ Damage in Cardiometabolic Disease.Biomolecules · 2018Review
- Dickkopf‑3 upregulation mediates the cardioprotective effects of curcumin on chronic heart failure.Molecular medicine reports · 2018Article
- Beneficial Effects of Galectin-3 Blockade in Vascular and Aortic Valve Alterations in an Experimental Pressure Overload Model.International journal of molecular sciences · 2017Article
- Thrombospondins: A Role in Cardiovascular Disease.International journal of molecular sciences · 2017Review
- Role for Galectin-3 in Calcific Aortic Valve Stenosis.Journal of the American Heart Association · 2016Observational
- Thrombospondins in the transition from myocardial infarction to heart failure.Journal of molecular and cellular cardiology · 2016Review
- RNA Profiling in Human and Murine Transplanted Hearts: Identification and Validation of Therapeutic Targets for Acute Cardiac and Renal Allograft Rejection.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2016Article
- Invoking the power of thrombospondins: regulation of thrombospondins expression.Matrix biology : journal of the International Society for Matrix Biology · 2014Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsThe cardiac extracellular matrix is highly involved in regulating inflammation, remodelling, and function of the heart. Whether matrix alterations relate to the degree of inflammation, fibrosis, and overall rejection in the human transplanted heart remained, until now, unknown. METHODS AND
resultsExpression of matricellular proteins, proteoglycans, and metalloproteinases (MMPs) and their inhibitors (TIMPs) were investigated in serial endomyocardial biopsies (n = 102), in a cohort of 39 patients within the first year after cardiac transplantation. Out of 15 matrix-related proteins, intragraft transcript and protein levels of syndecan-1 and MMP-9 showed a strong association with the degree of cardiac allograft rejection (CAR), the expression of pro-inflammatory cytokines tumour necrosis factor (TNF)-α, interleukin (IL)-6 and transforming growth factor (TGF)-β, and with infiltrating CD3⁺ T-cells and CD68⁺ monocytes. In addition, SPARC, CTGF, TSP-2, MMP-14, TIMP-1, Testican-1, TSP-1, Syndecan-1, MMP-2, -9, and -14, as well as IL-6 and TGF-β transcript levels and inflammatory infiltrates all strongly relate to collagen expression in the transplanted heart. More importantly, receiver operating characteristic curve analysis demonstrated that syndecan-1 and MMP-9 transcript levels had the highest area under the curve (0.969 and 0.981, respectively), thereby identifying both as a potential decision-making tool to discriminate rejecting from non-rejecting hearts.
conclusionOut of 15 matrix-related proteins, we identified synd-1 and MMP-9 intragraft transcript levels of as strong predictors of human CAR. In addition, a multitude of non-structural matrix-related proteins closely associate with collagen expression in the transplanted heart. Therefore, we are convinced that these findings deserve further investigation and are likely to be of clinical value to prevent human CAR.
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