ArticleThe Journal of pharmacology and experimental therapeutics2022
A Potent Inhibitor of Aminopeptidase P2 Reduces Reperfusion Injury in Models of Myocardial Infarction and Stroke.
Article in The Journal of pharmacology and experimental therapeutics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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
1 citing paper in PubMed, 1 citations in OpenAlex.
- Stroke Related Brain-Heart Crosstalk: Pathophysiology, Clinical Implications, and Underlying Mechanisms.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Review
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
During a myocardial infarction or ischemic stroke, blood flow to the heart or brain is partially blocked. This results in reduced delivery of oxygen and nutrients and, ultimately, tissue damage. Initial treatment involves removing the clot and restoring blood flow (reperfusion). However, this treatment is not as effective as one would hope because the reperfusion process itself can cause a different type of damage (reperfusion injury) that contributes up to 50% of the total damage. Bradykinin is an autocoid that is released from blood vessel endothelial cells during ischemia and reperfusion and has the potential to prevent reperfusion injury. However, bradykinin is rapidly inactivated by enzymes on endothelial cells, limiting its beneficial effects. One of these enzymes is aminopeptidase P2. We designed a potent and specific inhibitor of aminopeptidase P2 called ST-115, [(
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Registered trials
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