ArticleJournal of cardiovascular translational research2025
p16
Article in Journal of cardiovascular translational research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Progress on Potential Therapeutic Targets for Sepsis-Related Cardiac Dysfunction: From Basic Research to Clinical Translation.ImmunoTargets and therapy · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
Severe sepsis can promote myocardial injury and cardiac dysfunction, but role of p16 in sepsis-induced myocardial injury remains undefined. PBMCs were collected from patients. Expression of inflammatory factors and NLRP3 pathway were detected by Western blotting and qPCR in WT and p16KO mice. Then detect cardiomyocyte apoptosis and ROS levels in vitro. Detailed pathways and mechanisms were revealed through quantitative proteomic analysis combined with GSEA and KEGG analysis. p16 was overexpressed in PBMCs of patient. p16 knockout alleviated cardiac dysfunction in LPS-induced mice and inhibited NLRP3 inflammasome pathway in vivo and in vitro. Quantitative proteomic analysis revealed that p16 knockout contributed to the activation of the PI3K/Akt pathway in LPS-induced cardiac injury. p16 knockout promoted activation of the PI3K/Akt pathway and ameliorated NLRP3 pathway inhibition and redox imbalance thus improving cardiac function in LPS-induced cardiomyopathy mice.
Indexed as
Identifiers
39809973What OpenQuestion holds
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.