ReviewCells2023
Ischemic Tolerance-A Way to Reduce the Extent of Ischemia-Reperfusion Damage.
Review in Cells, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
8 citing papers in PubMed, 17 citations in OpenAlex.
- SOD1 regulates CXCR4 transcription in cortical neurons for establishment of cerebral ischemic tolerance.Journal of advanced research · 2026Article
- The Perspective of Using Ischemic Tolerance in Clinical Practice.Biomedicines · 2026Review
- The Kinetics of Microcirculatory Dysfunction During Paclitaxel Application in an In Vivo Mouse Model.Journal of clinical medicine · 2025Article
- Effects of 10- and 30-minute Hepatic Ischemia on Total Protein, Albumin, Globulin Fractions, and LDH of Male Albino Rates; An Experimental Study.Archives of academic emergency medicine · 2025Article
- Yellow Wine Polyphenolic Compounds protect against myocardial ischemia-reperfusion injury in rats by activating Nrf2 nuclear translocation to regulate the balance of mitochondrial fission and fusion.Frontiers in cardiovascular medicine · 2025Article
- Potential therapeutic targets in the prevention of testicular ischemia-reperfusion injury.Frontiers in reproductive health · 2025Review
- Intermittent fasting induced cerebral ischemic tolerance altered gut microbiome and increased levels of short-chain fatty acids to a beneficial phenotype.Neurochemistry international · 2024Article
- Effects of Trehalose Preconditioning on H9C2 Cell Viability and Autophagy Activation in a Model of Donation after Circulatory Death for Heart Transplantation.Current issues in molecular biology · 2024Article
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 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Individual tissues have significantly different resistance to ischemia-reperfusion damage. There is still no adequate treatment for the consequences of ischemia-reperfusion damage. By utilizing ischemic tolerance, it is possible to achieve a significant reduction in the extent of the cell damage due to ischemia-reperfusion injury. Since ischemia-reperfusion damage usually occurs unexpectedly, the use of preconditioning is extremely limited. In contrast, postconditioning has wider possibilities for use in practice. In both cases, the activation of ischemic tolerance can also be achieved by the application of sublethal stress on a remote organ. Despite very encouraging and successful results in animal experiments, the clinical results have been disappointing so far. To avoid the factors that prevent the activation of ischemic tolerance, the solution has been to use blood plasma containing tolerance effectors. This plasma is taken from healthy donors in which, after exposure to two sublethal stresses within 48 h, effectors of ischemic tolerance occur in the plasma. Application of this activated plasma to recipient animals after the end of lethal ischemia prevents cell death and significantly reduces the consequences of ischemia-reperfusion damage. Until there is a clear chemical identification of the end products of ischemic tolerance, the simplest way of enhancing ischemic tolerance will be the preparation of activated plasma from young healthy donors with the possibility of its immediate use in recipients during the initial treatment.
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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 Socratic graph.