Evidence map›Paper›PMID 33421567›Full record

ArticleJournal of the American College of Surgeons2021

Effect of Mitochondrial Antioxidant (Mito-TEMPO) on Burn-Induced Cardiac Dysfunction.

Jake J Wen, Taylor P Williams, Claire B Cummins, Kayla M Colvill, Geetha L Radhakrishnan, Ravi S Radhakrishnan

Open access · greenAbstract read
In one paragraph

Article in Journal of the American College of Surgeons, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.7field-weighted citation impact, top 10% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

13 citing papers in PubMed, 24 citations in OpenAlex.

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  6. Mitochondrial Integrity Is Critical in Right Heart Failure Development.International journal of molecular sciences · 2023
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Jake J WenDepartment of Surgery, University of Texas Medical Branch, Galveston, TX.
Taylor P WilliamsDepartment of Surgery, University of Texas Medical Branch, Galveston, TX.
Claire B CumminsDepartment of Surgery, University of Texas Medical Branch, Galveston, TX.
Kayla M ColvillDepartment of Surgery, University of Texas Medical Branch, Galveston, TX.
Geetha L RadhakrishnanDepartment of Pediatrics, University of Texas Medical Branch, Galveston, TX.
Ravi S RadhakrishnanDepartment of Surgery, University of Texas Medical Branch, Galveston, TX; Department of Pediatrics, University of Texas Medical Branch, Galveston, TX. Electronic address: rsradhak@utmb.edu.
The University of Texas Medical Branch at Galveston · US

Funding

POSTDOCTORAL TRAINING IN TRAUMA &BURNST32GM008256 · NIGMS · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI Celeste Campbell Finnerty, Oscar E. Suman-Vejas · 1990 to 2026
$4.0M
NIGMS NIH HHS T32 GM008256
6 · The paper itself

Abstract

backgroundImbalance of oxidants/antioxidants results in heart failure, contributing to mortality after burn injury. Cardiac mitochondria are a prime source of reactive oxygen species (ROS), and a mitochondrial-specific antioxidant may improve burn-induced cardiomyopathy. We hypothesize that the mitochondrial-specific antioxidant, Triphenylphosphonium chloride (Mito-TEMPO), could protect cardiac function after burn. STUDY

designMale rats had a 60% total body surface area (TBSA) scald burn injury and were treated with/without Mito-TEMPO (7 mg/kg-1, intraperitoneal) and harvested at 24 hours post-burn. Echocardiography (ECHO) was used for measurement of heart function. Masson Trichrome and hematoxylin and eosin (H & E) staining were used for cardiac fibrosis and immune response. Qualitative polymerase chain reaction (qPCR) was used for mitochondrial DNA replication and gene expression.

resultsBurn-induced cardiac dysfunction, fibrosis, and mitochondrial damage were assessed by measurement of mitochondrial function, DNA replication, and DNA-encoded electron transport chain-related gene expression. Mito-TEMPO partially improved the abnormal parameters. Burn-induced cardiac dysfunction was associated with crosstalk between the NFE2L2-ARE pathway, PDE5A-PKG pathway, PARP1-POLG-mtDNA replication pathway, and mitochondrial SIRT signaling.

conclusionsMito-TEMPO reversed burn-induced cardiac dysfunction by rescuing cardiac mitochondrial dysfunction. Mitochondria-targeted antioxidants may be an effective therapy for burn-induced cardiac dysfunction.

Indexed as

AnimalsAntioxidantsBurnsDisease Models, AnimalEchocardiographyHeartHeart FailureHumansInjections, IntraperitonealMaleMitochondriaMyocardiumOrganophosphorus CompoundsPiperidinesRatsReactive Oxygen SpeciesAntioxidantsMitoTEMPOOrganophosphorus CompoundsPiperidinesReactive Oxygen Species

Identifiers

PMID33421567
PMCPMC8753741
OpenAlexW3119527327

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.