Evidence map›Paper›PMID 29180214›Full record

ArticleThe Journal of surgical research2017

Thioredoxin-1 attenuates sepsis-induced cardiomyopathy after cecal ligation and puncture in mice.

Rickesha L Wilson, Vaithinathan Selvaraju, Rajesh Lakshmanan, Mahesh Thirunavukkarasu, Jacob Campbell, David W McFadden, Nilanjana Maulik

Open access · greenAbstract read
In one paragraph

Article in The Journal of surgical research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

15 citing papers in PubMed, 26 citations in OpenAlex.

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  11. Roflumilast, a Phosphodiesterases-4 (PDE4) Inhibitor, Alleviates Sepsis‑induced Acute Kidney Injury.Medical science monitor : international medical journal of experimental and clinical research · 2020
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Rickesha L WilsonMolecular Cardiology and Angiogenesis Laboratory, University of Connecticut School of Medicine, Farmington, Connecticut; Department of Surgery, University of Connecticut School of Medicine, Farmington, Connecticut.
Vaithinathan SelvarajuMolecular Cardiology and Angiogenesis Laboratory, University of Connecticut School of Medicine, Farmington, Connecticut; Department of Surgery, University of Connecticut School of Medicine, Farmington, Connecticut.
Rajesh LakshmananMolecular Cardiology and Angiogenesis Laboratory, University of Connecticut School of Medicine, Farmington, Connecticut; Department of Surgery, University of Connecticut School of Medicine, Farmington, Connecticut.
Mahesh ThirunavukkarasuMolecular Cardiology and Angiogenesis Laboratory, University of Connecticut School of Medicine, Farmington, Connecticut; Department of Surgery, University of Connecticut School of Medicine, Farmington, Connecticut. Electronic address: mthirunavukkarasu@uchc.edu.
Jacob CampbellMolecular Cardiology and Angiogenesis Laboratory, University of Connecticut School of Medicine, Farmington, Connecticut; Department of Surgery, University of Connecticut School of Medicine, Farmington, Connecticut.
David W McFaddenDepartment of Surgery, University of Connecticut School of Medicine, Farmington, Connecticut.
Nilanjana MaulikMolecular Cardiology and Angiogenesis Laboratory, University of Connecticut School of Medicine, Farmington, Connecticut; Department of Surgery, University of Connecticut School of Medicine, Farmington, Connecticut. Electronic address: nmaulik@uchc.edu.
University of Connecticut · US

Funding

Angiogenic Regulators in Ischemic DisordersR01GM112957 · NIGMS · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI MAULIK, NILANJANA · 2015 to 2018
$1.7M
NIGMS NIH HHS R01 GM112957
6 · The paper itself

Abstract

backgroundSepsis is a leading cause of mortality among patients in intensive care units across the USA. Thioredoxin-1 (Trx-1) is an essential 12 kDa cytosolic protein that, apart from maintaining the cellular redox state, possesses multifunctional properties. In this study, we explored the possibility of controlling adverse myocardial depression by overexpression of Trx-1 in a mouse model of severe sepsis.

methodsAdult C57BL/6J and Trx-1

resultsEchocardiography analysis showed preserved cardiac function in the Trx-1

conclusionsOur results indicate that overexpression of Trx-1 attenuates cardiac dysfunction during CLP. The mechanism of action may involve reduction of oxidative stress, apoptosis, and vascular permeability through activation of Trx-1/HO-1 and anti-apoptotic protein survivin.

Indexed as

Capillary PermeabilityAldehydesAnimalsApoptosisCardiomyopathiesCarrier ProteinsCaspase 3Disease Models, AnimalEchocardiographyFemaleHeartHeme Oxygenase-1ImmunohistochemistryInhibitor of Apoptosis ProteinsMaleMice3-nitrotyrosine4-hydroxy-2-nonenalAldehydesBirc5 protein, mouseCarrier ProteinsCasp3 protein, mouseCaspase 3Heme Oxygenase-1Inhibitor of Apoptosis ProteinsRepressor ProteinsSurvivinThioredoxinsTxn1 protein, mouseTxnip protein, mouseTyrosineAngiogenesisCardiomyopathyOxidative stressRedoxSepsisThioredoxin-1

Identifiers

PMID29180214
PMCPMC7904090
OpenAlexW2739012862

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.