ReviewImmunotherapy2010
TGF-beta, IL-6, IL-17 and CTGF direct multiple pathologies of chronic cardiac allograft rejection.
Review in Immunotherapy, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
22 citing papers in PubMed, 49 citations in OpenAlex.
- Cellular and Molecular Aspects of Chronic Rejection.Results and problems in cell differentiation · 2026Review
- Clinical determinants and biomarkers associated with cardiac fibrosis after heart transplantation as assessed by magnetic resonance: Size matters.International journal of cardiology. Heart & vasculature · 2024Article
- The role of IL-17 family cytokines in cardiac fibrosis.Frontiers in cardiovascular medicine · 2024Review
- Matrix Metalloproteinases and Heart Transplantation-A Pathophysiological and Clinical View.Medicina (Kaunas, Lithuania) · 2023Review
- Impact of donor blood type on outcomes after prolonged allograft ischemic times.The Journal of thoracic and cardiovascular surgery · 2022Article
- Computational Analysis of Routine Biopsies Improves Diagnosis and Prediction of Cardiac Allograft Vasculopathy.Circulation · 2022Article
- Macrophage depletion of CMV latently infected donor hearts ameliorates recipient accelerated chronic rejection.Transplant infectious disease : an official journal of the Transplantation Society · 2021Article
- IL-6 Directed Therapy in Transplantation.Current transplantation reports · 2021Review
- Anti-IL-6 eluting immunomodulatory biomaterials prolong skin allograft survival.Scientific reports · 2019Article
- Donor biomarkers as predictors of organ use and recipient survival after neurologically deceased donor organ transplantation.Journal of critical care · 2018Article
- Chronic Kidney Disease Increases Atrial Fibrillation Inducibility: Involvement of Inflammation, Atrial Fibrosis, and Connexins.Frontiers in physiology · 2018Article
- Novel Application of Localized Nanodelivery of Anti-Interleukin-6 Protects Organ Transplant From Ischemia-Reperfusion Injuries.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2017Article
- The role of sildenafil in the development of transplant arteriosclerosis in rat aortic grafts.American journal of translational research · 2017Article
- Targeted complement inhibition and microvasculature in transplants: a therapeutic perspective.Clinical and experimental immunology · 2016Review
- Role of LPA and the Hippo pathway on apoptosis in salivary gland epithelial cells.Experimental & molecular medicine · 2014Article
- Tim-1-Fc suppresses chronic cardiac allograft rejection and vasculopathy by reducing IL-17 production.International journal of clinical and experimental pathology · 2014Article
- IL-13 signaling via IL-13Rα2 triggers TGF-β1-dependent allograft fibrosis.Transplantation research · 2013Article
- Matricellular proteins and matrix metalloproteinases mark the inflammatory and fibrotic response in human cardiac allograft rejection.European heart journal · 2013Article
- Interleukin-17 causes Rho-kinase-mediated endothelial dysfunction and hypertension.Cardiovascular research · 2013Article
- Recipient-derived EDA fibronectin promotes cardiac allograft fibrosis.The Journal of pathology · 2012Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Cardiac transplantation is an effective treatment for heart failure refractive to therapy. Although immunosuppressive therapeutics have increased first year survival rates, chronic rejection remains a significant barrier to long-term graft survival. Chronic rejection manifests as patchy interstitial fibrosis, vascular occlusion and progressive loss of graft function. Recent evidence from experimental and patient studies suggests that the development of cardiomyocyte hypertrophy is another hallmark of chronic cardiac allograft rejection. This pathologic hypertrophy is tightly linked to the immune cytokine IL-6, which promotes facets of chronic rejection in concert with TGF-beta and IL-17. These factors potentiate downstream mediators, such as CTGF, which promote the fibrosis associated with the disease. In this article, we summarize contemporary findings that have revealed several elements involved in the induction and progression of chronic rejection of cardiac allografts. Further efforts to elucidate the interplay between these factors may direct the development of targeted therapies for this disease.
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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.