Evidence map›Paper›PMID 33910093›Full record

ReviewFree radical biology & medicine2021

Therapeutic potential of targeting oxidative stress in diabetic cardiomyopathy.

Nikole J Byrne, Namakkal S Rajasekaran, E Dale Abel, Heiko Bugger

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Free radical biology & medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
91citing papers in PubMed, 1 pooled it
18.5field-weighted citation impact, top 1% 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

91 citing papers in PubMed, 1 synthesis or guideline pooled it, 165 citations in OpenAlex.

  1. Pooled it
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  12. Diabetes and cancer: therapeutic implications.Cardio-oncology (London, England) · 2026
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31 more citing papers are in PubMed but not listed here.

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

4 authors at 3 institutions in 2 countries.

Nikole J ByrneDivision of Cardiology, Medical University of Graz, Graz, Austria.
Namakkal S RajasekaranCardiac Aging & Redox Signaling Laboratory, Molecular and Cellular Pathology, Department of Pathology, Birmingham, AL, USA; Division of Cardiovascular Medicine, Department of Medicine, University of Utah School of Medicine, Salt Lake City, UT, USA; Center for Free Radical Biology, University of Alabama at Birmingham, Birmingham, AL, USA.
E Dale AbelFraternal Order of Eagles Diabetes Research Center, Division of Endocrinology and Metabolism, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City, USA.
Heiko BuggerDivision of Cardiology, Medical University of Graz, Graz, Austria. Electronic address: heiko.bugger@medunigraz.at.
Medical University of Graz · ATUniversity of Iowa · USUniversity of Utah · US

Funding

ANIMAL MODELS OF DIABETIC CARDIOVASCULAR COMPLICATIONSU01HL070525 · UNIVERSITY OF UTAH · 2001 to 2005
$3.7M
Insulin resistance and cardiac dysfunction in obesityR01HL073167 · UNIVERSITY OF UTAH · 2003 to 2005
$1.3M
NHLBI NIH HHS R01 HL073167NHLBI NIH HHS R01 HL118067NHLBI NIH HHS R61 HL141783NHLBI NIH HHS U01 HL070525NHLBI NIH HHS U01 HL087947NHLBI NIH HHS U54 HL112311NIA NIH HHS R03 AG042860NIDDK NIH HHS R24 DK092784
6 · The paper itself

Abstract

Even in the absence of coronary artery disease and hypertension, diabetes mellitus (DM) may increase the risk for heart failure development. This risk evolves from functional and structural alterations induced by diabetes in the heart, a cardiac entity termed diabetic cardiomyopathy (DbCM). Oxidative stress, defined as the imbalance of reactive oxygen species (ROS) has been increasingly proposed to contribute to the development of DbCM. There are several sources of ROS production including the mitochondria, NAD(P)H oxidase, xanthine oxidase, and uncoupled nitric oxide synthase. Overproduction of ROS in DbCM is thought to be counterbalanced by elevated antioxidant defense enzymes such as catalase and superoxide dismutase. Excess ROS in the cardiomyocyte results in further ROS production, mitochondrial DNA damage, lipid peroxidation, post-translational modifications of proteins and ultimately cell death and cardiac dysfunction. Furthermore, ROS modulates transcription factors responsible for expression of antioxidant enzymes. Lastly, evidence exists that several pharmacological agents may convey cardiovascular benefit by antioxidant mechanisms. As such, increasing our understanding of the pathways that lead to increased ROS production and impaired antioxidant defense may enable the development of therapeutic strategies against the progression of DbCM. Herein, we review the current knowledge about causes and consequences of ROS in DbCM, as well as the therapeutic potential and strategies of targeting oxidative stress in the diabetic heart.

Indexed as

Diabetes MellitusDiabetic CardiomyopathiesAntioxidantsHumansNADPH OxidasesOxidative StressReactive Oxygen SpeciesAntioxidantsNADPH OxidasesReactive Oxygen SpeciesDiabetesDiabetic cardiomyopathyDiabetic heartMitochondriaOxidative stressReactive oxygen species

Identifiers

PMID33910093
PMCPMC8285002
OpenAlexW3157906588

What Socratic 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 Socratic graph.