Evidence map›Paper›PMID 29540307›Full record

ArticleFree radical biology & medicine2018

Oxidative cross-linking of proteins to DNA following ischemia-reperfusion injury.

Arnold Groehler, Stefan Kren, Qinglu Li, Maggie Robledo-Villafane, Joshua Schmidt, Mary Garry, Natalia Tretyakova

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Free radical biology & medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

18 citing papers in PubMed, 31 citations in OpenAlex.

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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 2 institutions in 1 country.

Arnold GroehlerDepartment of Medicinal Chemistry, University of Minnesota, 8-101 Weaver Densford Hall, 308 Harvard Street SE, Minneapolis, MN 55455, USA.
Stefan KrenLillehei Heart Institute, University of Minnesota, 4-165 CCRB, 2231 6th Street SE, Minneapolis, MN 55455, USA.
Qinglu LiLillehei Heart Institute, University of Minnesota, 4-165 CCRB, 2231 6th Street SE, Minneapolis, MN 55455, USA.
Maggie Robledo-VillafaneLillehei Heart Institute, University of Minnesota, 4-165 CCRB, 2231 6th Street SE, Minneapolis, MN 55455, USA.
Joshua SchmidtDepartment of Medicinal Chemistry, University of Minnesota, 8-101 Weaver Densford Hall, 308 Harvard Street SE, Minneapolis, MN 55455, USA.
Mary GarryLillehei Heart Institute, University of Minnesota, 4-165 CCRB, 2231 6th Street SE, Minneapolis, MN 55455, USA.
Natalia TretyakovaDepartment of Medicinal Chemistry, University of Minnesota, 8-101 Weaver Densford Hall, 308 Harvard Street SE, Minneapolis, MN 55455, USA; Masonic Cancer Center, University of Minnesota, 2-147 CCRB, 2231 6th Street SE, Minneapolis, MN 55455, USA. Electronic address: trety001@umn.edu.
University of Minnesota · USMinneapolis Heart Institute Foundation · US

Funding

DNA Protein Cross-Links:Cellular Effects and Repair MechanismsR01ES023350 · NIEHS · UNIVERSITY OF MINNESOTA · PI CAMPBELL, COLIN R, TRETYAKOVA, NATALIA Y · 2014 to 2023
$5.0M
NIEHS NIH HHS R01 ES023350
6 · The paper itself

Abstract

Myocardial infarction (MI) is a life-threatening condition that can occur when blood flow to the heart is interrupted due to a blockage in one or more of the coronary vessels. Current treatments of MI rapidly restore blood flow to the affected myocardium using thrombolytic agents or angioplasty. Adverse effects including inflammation, tissue necrosis, and ventricular dysfunction are, however, not uncommon following reperfusion therapy. These conditions are thought to be caused by a sudden influx of reactive oxygen species (ROS) to the affected myocardium. We employed the model of left anterior descending artery ligation/reperfusion surgery in a rat model to show that ischemia/reperfusion injury is associated with the formation of toxic DNA-protein cross-links (DPCs) in cardiomyocytes. Mass spectrometry based experiments have revealed that these conjugates were formed by a free radical mechanism and involved thymidine residues of DNA and tyrosine side chains of proteins (dT-Tyr). Quantitative proteomics experiments have identified nearly 90 proteins participating in hydroxyl radical-induced DPC formation, including ROS scavengers, contractile proteins, and regulators of apoptosis. Global proteome changes were less pronounced and included increased expression of mitochondrial proteins required for aerobic respiration and biomarkers of sarcomere breakdown following ischemia/reperfusion injury. Overall, our results are consistent with a model where sudden return of oxygen to ischemic tissues induces oxidative stress, inflammation, and the formation of DNA-protein cross-links that may contribute to reperfusion injury by desregulating gene expression and inducing cardiomyocyte death.

Indexed as

AnimalsDNA AdductsFree RadicalsMaleMyocardial Reperfusion InjuryMyocytes, CardiacOxidative StressProteomicsRatsRats, Sprague-DawleyReactive Oxygen SpeciesThymidineTyrosineDNA AdductsFree RadicalsReactive Oxygen SpeciesThymidineTyrosineCardiomyocytesDNA-protein cross-linkingIschemia-reperfusion injuryMass spectrometry based proteomicsReactive oxygen species

Identifiers

PMID29540307
PMCPMC5940493
OpenAlexW2794333766

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.