Evidence map›Paper›PMID 30940158›Full record

ArticleJournal of translational medicine2019

FNDC5 attenuates obesity-induced cardiac hypertrophy by inactivating JAK2/STAT3-associated inflammation and oxidative stress.

Zhi Geng, Wen-Yong Fan, Bing Zhou, Chao Ye, Ying Tong, Ye-Bo Zhou, Xiao-Qing Xiong

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
6.6field-weighted citation impact, top 3% 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

41 citing papers in PubMed, 63 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 3 institutions in 1 country.

Zhi GengDepartment of Cardiac Surgery, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, 210011, Jiangsu, China.
Wen-Yong FanState Key Laboratory of Medical Neurobiology, Department of Physiology and Biophysics, School of Life Sciences and Collaborative Innovation Centre for Brain Science, Fudan University, Shanghai, 200438, China.
Bing ZhouKey Laboratory of Cardiovascular Disease and Molecular Intervention, Department of Physiology, Nanjing Medical University, 101 Longmian Avenue, Nanjing, 211166, Jiangsu, China.
Chao YeKey Laboratory of Cardiovascular Disease and Molecular Intervention, Department of Physiology, Nanjing Medical University, 101 Longmian Avenue, Nanjing, 211166, Jiangsu, China.
Ying TongKey Laboratory of Cardiovascular Disease and Molecular Intervention, Department of Physiology, Nanjing Medical University, 101 Longmian Avenue, Nanjing, 211166, Jiangsu, China.
Ye-Bo ZhouKey Laboratory of Cardiovascular Disease and Molecular Intervention, Department of Physiology, Nanjing Medical University, 101 Longmian Avenue, Nanjing, 211166, Jiangsu, China.
Xiao-Qing XiongKey Laboratory of Cardiovascular Disease and Molecular Intervention, Department of Physiology, Nanjing Medical University, 101 Longmian Avenue, Nanjing, 211166, Jiangsu, China. xqxiong@njmu.edu.cn.ORCID 0000-0003-4143-5097
Nanjing Medical University · CNFudan University · CNSecond Affiliated Hospital of Nanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundChronic low-grade inflammation and oxidative stress play important roles in the development of obesity-induced cardiac hypertrophy. Here, we investigated the role of Fibronectin type III domain containing 5 (FNDC5) in cardiac inflammation and oxidative stress in obesity-induced cardiac hypertrophy.

methodsMale wild-type and FNDC5

resultsHigh fat diet manifested significant increases in body weight and cardiac hypertrophy marker genes expression, while FNDC5 deficiency aggravated cardiac hypertrophy evidenced by increased Nppa, Nppb and Myh7 mRNA level and cardiomyocytes area, in association with enhanced cardiac inflammatory cytokines expression, oxidative stress level and JAK2/STAT3 activation in HFD-fed mice. FNDC5 deficiency in primary cardiomyocytes or FNDC5 knockdown in H9c2 cells enhanced PA-induced inflammatory responses and NOX4 expression. Exogenous FNDC5 pretreatment attenuated PA-induced cardiomyocytes hypertrophy, inflammatory cytokines up-regulation and oxidative stress in primary cardiomyocytes and H9c2 cells. FNDC5 overexpression attenuated cardiac hypertrophy as well as cardiac inflammation and oxidative stress in HFD-fed mice.

conclusionsFNDC5 attenuates obesity-induced cardiac hypertrophy by inactivating JAK2/STAT3 associated-cardiac inflammation and oxidative stress. The cardio-protective role of FNDC5 shed light on future therapeutic interventions in obesity and related cardiovascular complications.

Indexed as

AnimalsCardiomegalyDiet, High-FatDown-RegulationFibronectinsInflammationJanus Kinase 2MaleMiceMice, Inbred C57BLMice, KnockoutMyocytes, CardiacObesityOxidative StressSignal TransductionSTAT3 Transcription FactorFibronectinsFNDC5 protein, mouseJAK2 protein, humanJanus Kinase 2STAT3 protein, humanSTAT3 Transcription FactorCardiac hypertrophyFNDC5InflammationObesityOxidative stress

Identifiers

PMID30940158
PMCPMC6444535
OpenAlexW2944682852

What OpenQuestion holds

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LicenceCC BY
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.