ArticlePPAR research2013
Doxorubicin-Induced Cardiac Toxicity Is Mediated by Lowering of Peroxisome Proliferator-Activated Receptor δ Expression in Rats.
Article in PPAR research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed, 23 citations in OpenAlex.
- Vardenafil Alleviates Doxorubicin-Induced Cardiotoxicity Associated with Restoration of the AMPK/SIRT1 Signaling Pathway.Biomedicines · 2026Article
- Liraglutide Pretreatment Does Not Improve Acute Doxorubicin-Induced Cardiotoxicity in Rats.International journal of molecular sciences · 2024Article
- Role of oxidative stress and inflammation-related signaling pathways in doxorubicin-induced cardiomyopathy.Cell communication and signaling : CCS · 2023Review
- The attenuation effect of low piperinePharmaceutical biology · 2022Article
- Review
- Targeting PPARs Signaling Pathways in Cardiotoxicity by Natural Compounds.Cardiovascular toxicology · 2022Review
- Mitochondrial Determinants of Doxorubicin-Induced Cardiomyopathy.Circulation research · 2020Review
- Review
- PPARNuclear receptor research · 2018Article
- A rapid screening system evaluates novel inhibitors of DNA methylation and suggests F-box proteins as potential therapeutic targets for high-risk neuroblastoma.Targeted oncology · 2015Article
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
The present study investigates the changes of peroxisome proliferator-activated receptors δ (PPAR δ ) expression and troponin phosphorylation in heart of rats which were treated with doxorubicin (DOX). Wistar rats which were treated with DOX according to a previous method. The protein levels of PPAR δ and troponin phosphorylation were measured using Western blot. The PPAR δ expression in heart was markedly reduced in DOX-treated rats showing a marked decrease in cardiac dP/dT and cardiac output. Also, cardiac troponin phosphorylation was lowered in DOX-treated rats. Meanwhile, combined treatment with the agonist of PPAR δ (GW0742) reversed the decrease of cardiac dP/dT and cardiac output in DOX-treated rats. Then, primary cultured cardiomyocytes from neonatal rats were used to measure the changes of calcium concentration in cells. In addition to both decrease of PPAR δ expression and troponin phosphorylation in neonatal cardiomyocytes by DOX, a marked decrease of calcium concentration was also observed. Our results suggest the mediation of cardiac PPAR δ in DOX-induced cardiotoxicity in rats. Thus, activation of PPAR δ may restore the expression of p-TnI and the cardiac performance in DOX-induced cardio toxicity in rats.
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.