Evidence map›Paper›PMID 26577173›Full record

ArticleFree radical biology & medicine2016

Therapeutic inhibition of mitochondrial reactive oxygen species with mito-TEMPO reduces diabetic cardiomyopathy.

Rui Ni, Ting Cao, Sidong Xiong, Jian Ma, Guo-Chang Fan, James C Lacefield, Yanrong Lu, Sydney Le Tissier, Tianqing Peng

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

Article in Free radical biology & medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 171 papers.

0numbers the graph read from it
0cells of the map it votes in
171citing papers in PubMed
6.9field-weighted citation impact, top 2% 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

171 citing papers in PubMed, 281 citations in OpenAlex.

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111 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

9 authors at 5 institutions in 3 countries.

Rui NiJiangsu Key Laboratory of Infection and Immunity, Institutes of Biology and Medical Sciences, Soochow University, Suzhou, Jiangsu Province 215123, China; Critical Illness Research, Lawson Health Research Institute, London Health Sciences Centre, VRL 6th Floor, A6-140, 800 Commissioners Road, London, Ont., Canada N6A 4G5; Departments of Medicine and Pathology, The University of Western Ontario, London, Ont., Canada N6A 4G5.
Ting CaoJiangsu Key Laboratory of Infection and Immunity, Institutes of Biology and Medical Sciences, Soochow University, Suzhou, Jiangsu Province 215123, China.
Sidong XiongJiangsu Key Laboratory of Infection and Immunity, Institutes of Biology and Medical Sciences, Soochow University, Suzhou, Jiangsu Province 215123, China.
Jian MaCritical Illness Research, Lawson Health Research Institute, London Health Sciences Centre, VRL 6th Floor, A6-140, 800 Commissioners Road, London, Ont., Canada N6A 4G5; Departments of Medicine and Pathology, The University of Western Ontario, London, Ont., Canada N6A 4G5.
Guo-Chang FanDepartment of Pharmacology and Cell Biophysics, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA.
James C LacefieldElectrical and Computer Engineering, Medical Biophysics, Robarts Research Institute, University of Western Ontario, London, Ont., Canada N6A 4G5.
Yanrong LuKey Laboratory of Transplant Engineering and Immunology, Ministry of Health; Regenerative Medicine Research Center, West China Hospital, Sichuan University, Chengdu 610041, China.
Sydney Le TissierCritical Illness Research, Lawson Health Research Institute, London Health Sciences Centre, VRL 6th Floor, A6-140, 800 Commissioners Road, London, Ont., Canada N6A 4G5.
Tianqing PengJiangsu Key Laboratory of Infection and Immunity, Institutes of Biology and Medical Sciences, Soochow University, Suzhou, Jiangsu Province 215123, China; Critical Illness Research, Lawson Health Research Institute, London Health Sciences Centre, VRL 6th Floor, A6-140, 800 Commissioners Road, London, Ont., Canada N6A 4G5; Departments of Medicine and Pathology, The University of Western Ontario, London, Ont., Canada N6A 4G5. Electronic address: tpeng2@suda.edu.cn.
Western University · CALondon Health Sciences Centre · CASoochow University · CNSichuan University · CNUniversity of Cincinnati Medical Center · US

Funding

Roles of Hsp20-Exosomes in Myocardial AngiogenesisR01HL087861 · NHLBI · UNIVERSITY OF CINCINNATI · PI FAN, GUO-CHANG · 2007 to 2017
$4.2M
Duplex miR-223 and Exosomes in SepsisR01GM112930 · NIGMS · UNIVERSITY OF CINCINNATI · PI FAN, GUO-CHANG · 2015 to 2018
$1.2M
Canadian Institutes of Health Research MOP-133657NHLBI NIH HHS HL-087861NHLBI NIH HHS R01 HL087861NIGMS NIH HHS GM-112930NIGMS NIH HHS R01 GM112930
6 · The paper itself

Abstract

aimsThe mitochondria are important sources of reactive oxygen species (ROS) in the heart. Mitochondrial ROS production has been implicated in the pathogenesis of diabetic cardiomyopathy, suggesting that therapeutic strategies specifically targeting mitochondrial ROS may have benefit in this disease. We investigated the therapeutic effects of mitochondria-targeted antioxidant mito-TEMPO on diabetic cardiomyopathy.

methodsThe mitochondria-targeted antioxidant mito-TEMPO was administrated after diabetes onset in a mouse model of streptozotocin-induced type-1 diabetes and type-2 diabetic db/db mice. Cardiac adverse changes were analyzed and myocardial function assessed. Cultured adult cardiomyocytes were stimulated with high glucose, and mitochondrial superoxide generation and cell death were measured.

resultsIncubation with high glucose increased mitochondria superoxide generation in cultured cardiomyocytes, which was prevented by mito-TEMPO. Co-incubation with mito-TEMPO abrogated high glucose-induced cell death. Mitochondrial ROS generation, and intracellular oxidative stress levels were induced in both type-1 and type-2 diabetic mouse hearts. Daily injection of mito-TEMPO for 30 days inhibited mitochondrial ROS generation, prevented intracellular oxidative stress levels, decreased apoptosis and reduced myocardial hypertrophy in diabetic hearts, leading to improvement of myocardial function in both type-1 and type-2 diabetic mice. Incubation with mito-TEMPO or inhibition of Nox2-containing NADPH oxidase prevented oxidative stress levels and cell death in high glucose-stimulated cardiomyocytes. Mechanistic study revealed that the protective effects of mito-TEMPO were associated with down-regulation of ERK1/2 phosphorylation.

conclusionsTherapeutic inhibition of mitochondrial ROS by mito-TEMPO reduced adverse cardiac changes and mitigated myocardial dysfunction in diabetic mice. Thus, mitochondria-targeted antioxidants may be an effective therapy for diabetic cardiac complications.

Indexed as

AnimalsAntioxidantsDiabetes Mellitus, ExperimentalDiabetic CardiomyopathiesExtracellular Signal-Regulated MAP KinasesMiceMice, Inbred C57BLMitochondriaOrganophosphorus CompoundsOxidative StressPiperidinesReactive Oxygen SpeciesSuperoxidesAntioxidantsExtracellular Signal-Regulated MAP KinasesMitoTEMPOOrganophosphorus CompoundsPiperidinesReactive Oxygen SpeciesSuperoxidesDiabetic cardiomyopathyERK1/2MitochondriaMito-TEMPOReactive oxygen species

Identifiers

PMID26577173
PMCPMC5066872
OpenAlexW2159829960

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Registered trials

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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.