Evidence map›Paper›PMID 28888894›Full record

ArticleRedox biology2018

Exercise intervention attenuates hyperhomocysteinemia-induced aortic endothelial oxidative injury by regulating SIRT1 through mitigating NADPH oxidase/LOX-1 signaling.

Shih-Hung Chan, Ching-Hsia Hung, Jhih-Yuan Shih, Pei-Ming Chu, Yung-Hsin Cheng, Huei-Chen Lin, Pei-Ling Hsieh, Kun-Ling Tsai

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

Article in Redox biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
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

38 citing papers in PubMed, 1 synthesis or guideline pooled it, 79 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

8 authors at 6 institutions in 1 country.

Shih-Hung ChanDepartment of Internal Medicine, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Ching-Hsia HungDepartment of Physical Therapy, College of Medicine, National Cheng Kung University, Tainan, Taiwan; Institute of Allied Health Sciences, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Jhih-Yuan ShihDepartment of Internal Medicine, Chi-Mei Hospital, Tainan, Taiwan.
Pei-Ming ChuDepartment of Anatomy, School of Medicine, China Medical University, Taichung, Taiwan.
Yung-Hsin ChengDepartment of Education and Research, Taipei City Hospital, Taipei, Taiwan.
Huei-Chen LinInstitute of Allied Health Sciences, College of Medicine, National Cheng Kung University, Tainan, Taiwan; Department of Physical Therapy, Shu-Zen Junior College of Medicine and Management, Taiwan.
Pei-Ling HsiehInstitute of Oral Sciences, Chung Shan Medical University, Taichung, Taiwan.
Kun-Ling TsaiDepartment of Physical Therapy, College of Medicine, National Cheng Kung University, Tainan, Taiwan. Electronic address: kunlingtsai@mail.ncku.edu.tw.
National Cheng Kung University · TWChi Mei Medical Center · TWChina Medical University · TWChung Shan Medical University · TWNational Cheng Kung University Hospital · TWTaipei City Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Coronary artery disease (CAD) is a critical cardiovascular disease and a cause of high morbidity and mortality in this world. Hyperhomocysteinemia (HHcy) has been suggested as a risk factor for CAD. In addition, SIRT1 (sirtuin 1) has been reported to play a protective role in a variety of diseases, especially in the cardiovascular system. The main purpose of this study was to investigate the effects of exercise training on apoptosis and inflammation in HHcy animals. We also tested whether exercise protected against Hhcy-induced dysfunction of endothelium through modulation of SIRT1. C57BL mice (8 in each group) were fed with or without 1% L-methionine (w/w) in water for 4 months to induce HHcy. We found that Hhcy repressed SIRT1 and AMPK expression and increased NADPH oxidase activity. Plasma MDA, endothelium LOX-1 and p-p38 were up-regulated by Hhcy induction. NF-κB and it downstream molecules were activated under Hhcy situation, thereby promoting pro-inflammatory responses. Moreover, we also reported that Hhcy caused endothelium apoptosis involving Akt inhibition and mitochondria-dependent apoptotic pathways. Exercise training significantly protected against endothelium from Hhcy caused oxidative injuries. In addition, EX527 (SIRT1 inhibitor) reduced the therapeutic effects by exercise. Our results had indicated that exercise training prevent the development of atherosclerosis through SIRT1 activation and oxidative stress inhibition under Hhcy situation.

Indexed as

AnimalsAtherosclerosisCarbazolesEndothelium, VascularHyperhomocysteinemiaMaleMalondialdehydeMethionineMiceMice, Inbred C57BLNADPH Oxidase 1NeuropeptidesNF-kappa BOxidative StressPhysical Conditioning, Animalrac1 GTP-Binding Protein6-chloro-2,3,4,9-tetrahydro-1H-carbazole-1-carboxamideCarbazolesMalondialdehydeMethionineNADPH Oxidase 1NeuropeptidesNF-kappa BOlr1 protein, mouserac1 GTP-Binding ProteinRac1 protein, mouseScavenger Receptors, Class ESirtuin 1Superoxide DismutaseCoronary artery diseaseHyperhomocysteinemiaOxidative stressSirtuin 1

Identifiers

PMID28888894
PMCPMC5596261
OpenAlexW2747789678

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.