ArticleJournal of the American College of Surgeons2023
PARP1 Inhibition and Effect on Burn Injury-Induced Inflammatory Response and Cardiac Function.
Article in Journal of the American College of Surgeons, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
2 citing papers in PubMed, 4 citations in OpenAlex.
- Burns: The "Fuse" That Ignites Organ Crisis - A Narrative Review of Mechanisms and Crosstalk in Post-Burn MODS.Journal of inflammation research · 2026Review
- Discovery of the PARP1 Inhibitors from Natural Compounds Using Structure-Based Virtual Screening and Bioactivity Evaluation.Medicinal chemistry (Shariqah (United Arab Emirates)) · 2026Article
Corrections and comments
- Commented on byDiscussion.2023
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
backgroundBurn injury induces multiple signaling pathways leading to a significant inflammatory storm that adversely affects multiple organs, including the heart. Poly (ADP-ribose) polymerase inhibitor 1 (PARP1) inhibition, with specific agents such as N-(5,6-Dihydro-6-oxo-2-phenanthridinyl)-2-acetamide (PJ34), is effective in reducing oxidative stress and cytokine expression in the heart. We hypothesized that PARP1 inhibition would reduce inflammatory signaling and protect against burn injury-induced cardiac dysfunction. STUDY
designMale Sprague-Dawley rats (8 weeks old, 300 to 350 g) were randomly assigned to sham injury (Sham), 60% total body surface area burn (24 hours post burn), or 60% total body surface area burn with intraperitoneal administration of PJ34 (20 mg/kg, 24 hours post burn + PJ34) and sacrificed 24 hours after injury. Cardiac function was determined using Vevo 2100 echocardiography. Genetic expression of 84 specific toll-like receptor-mediated signal transduction and innate immunity genes were examined using microarray to evaluate cardiac tissue. Qiagen GeneGlobe Data Analysis Center was used to analyze expression, and genetic clustering was performed using TreeView V2.0.8 software. Real-time quantitative polymerase chain reaction was used to validate identified differentially expressed genes.
resultsBurn injury significantly altered multiple genes in the toll-like receptor signaling, interleukin-17 signaling, tumor necrosis factor signaling, and nuclear factor-κB signaling pathways and led to significant cardiac dysfunction. PARP1 inhibition with PJ34 normalized these signaling pathways to sham levels as well as improved cardiac function to sham levels.
conclusionsPARP1 inhibition normalizes multiple inflammatory pathways that are altered after burn injury and improves cardiac dysfunction. PARP1 pathway inhibition may provide a novel methodology to normalize multiple burn injury-induced inflammatory pathways in the heart.
Indexed as
Identifiers
What 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.