ArticleJournal of inflammation (London, England)2010
Anti-inflammatory treatment strategies for ischemia/reperfusion injury in transplantation.
Article in Journal of inflammation (London, England), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 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.
The trial behind it
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
60 citing papers in PubMed, 157 citations in OpenAlex.
- How Cytokines Regulate Immune Response Toward Chronic Allograft Rejection?Results and problems in cell differentiation · 2026Review
- Overexpression of PGC-1α reduces inflammation and protects against focal cerebral ischaemia/reperfusion injury.Archives of medical science : AMS · 2026Article
- A review of protective effects ofFrontiers in pharmacology · 2026Review
- Article
- Review
- Amyloid β1-40 Predicts Long-Term Mortality Rate in Patients With Acute Myocardial Infarction.Journal of the American Heart Association · 2025Article
- Hypothermic machine perfusion in uterus transplantation in a porcine model: A proof of concept and the first results in graft preservation.Acta obstetricia et gynecologica Scandinavica · 2025Article
- Alterations in the inflammatory homeostasis of aging-related cardiac dysfunction and Alzheimer's diseases.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Review
- Anthraquinones fromDrug design, development and therapy · 2025Review
- The Protective Role of Molecular Hydrogen in Ischemia/Reperfusion Injury.International journal of molecular sciences · 2024Review
- Effects of therapeutic hypercapnia on the expression and function of γδT cells in transplanted lungs in rats.Immunity, inflammation and disease · 2024Article
- Fluid shear stress induced-endothelial phenotypic transition contributes to cerebral ischemia-reperfusion injury and repair.APL bioengineering · 2024Article
- Comprehensive molecular and cellular characterization of endoplasmic reticulum stress-related key genes in renal ischemia/reperfusion injury.Frontiers in immunology · 2024Article
- Article
- Zebrafish as a high throughput model for organ preservation and transplantation research.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023Article
- Effects of remote ischemic postconditioning on hepatic injury in lipopolysaccharide-induced endotoxemic rats.Korean journal of anesthesiology · 2023Article
- Key hepatoprotective roles of mitochondria in liver regeneration.American journal of physiology. Gastrointestinal and liver physiology · 2023Review
- Inflammation balance in skeletal muscle damage and repair.Frontiers in immunology · 2023Review
- Cytokines Removal DuringTransplant international : official journal of the European Society for Organ Transplantation · 2023Article
- Targeting IL-6 to prevent cardiac allograft rejection.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammatory reactions in the graft have a pivotal influence on acute as well as long-term graft function. The main reasons for an inflammatory reaction of the graft tissue are rejection episodes, infections as well as ischemia/reperfusion (I/R) injury. The latter is of particular interest as it affects every solid organ during the process of transplantation. I/R injury impairs acute as well as long-term graft function and is associated with an increased number of acute rejection episodes that again affect long-term graft outcome.I/R injury is the result of ATP depletion during prolonged hypoxia. Further tissue damage results from the reperfusion of the tissue after the ischemic insult. Adaptive cellular responses activate the innate immune system with its Toll-like receptors and the complement system as well as the adaptive immune system. This results in a profound inflammatory tissue reaction with immune cells infiltrating the tissue. The damage is mediated by various cytokines, chemokines, adhesion molecules, and compounds of the extracellular matrix. The expression of these factors is regulated by specific transcription factors with NF-kappaB being one of the key modulators of inflammation.Strategies to prevent or treat I/R injury include blockade of cytokines/chemokines, adhesion molecules, NF-kappaB, specific MAP kinases, metalloproteinases, induction of protective genes, and modulation of the innate immune system. Furthermore, preconditioning of the donor is an area of intense research. Here pharmacological treatment as well as new additives to conventional cold storage solutions have been analyzed together with new techniques for the perfusion of grafts, or methods of normothermic storage that would avoid the problem of cold damage and graft ischemia.However, the number of clinical trials in the field of I/R injury is limited as compared to the large body of experimental knowledge that accumulated during recent years in the field of I/R injury. Future activities in the treatment of I/R injury should focus on the translation of experimental protocols into clinical trials in order to reduce I/R injury and, thus, improve short- as well as long-term graft outcome.
Identifiers
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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.