ArticleFEBS open bio2020
PDRPS7 protects cardiac cells from hypoxia/reoxygenation injury through inactivation of JNKs.
Article in FEBS open bio, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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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Who cites it
3 citing papers in PubMed, 6 citations in OpenAlex.
- Article
- Transcription factor JDP2 activates PDE4B to participate in hypoxia/reoxygenation-induced H9c2 cell injury.Experimental and therapeutic medicine · 2022Article
- Mechanism and Protective Effect ofFrontiers in pharmacology · 2022Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myocardial ischemia/reperfusion (I/R) injury is a major complication of reperfusion therapy in myocardial infarction. Ischemic myocardium produces a variety of peptides. We recently identified PDRPS7 as a novel peptide in cardiomyocytes that can be induced by hypoxia. However, the role of PDRPS7 is unknown. Here, we investigated the effects of PDRPS7 on hypoxia/reoxygenation (H/R)-induced injury in rat cardiomyoblast H9c2 cells and NRCMs. We found that PDRPS7 improved cell survival and attenuated lactate dehydrogenase leakage following H/R in H9c2 cells and NRCMs. PDRPS7 also alleviated H/R-induced pulsation reduction in NRCMs. Moreover, H/R-induced cell apoptosis was decreased in the presence of PDRPS7. H/R-induced reactive oxygen species generation was reduced by PDRPS7; in addition, PDRPS7 did not impact H
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