Evidence map›Paper›PMID 29138395›Full record

ArticleNature communications2017

Myokine mediated muscle-kidney crosstalk suppresses metabolic reprogramming and fibrosis in damaged kidneys.

Hui Peng, Qianqian Wang, Tanqi Lou, Jun Qin, Sungyun Jung, Vivekananda Shetty, Feng Li, Yanlin Wang, Xin-Hua Feng, William E Mitch and 2 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers.

0numbers the graph read from it
0cells of the map it votes in
99citing papers in PubMed
7.9field-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

99 citing papers in PubMed, 185 citations in OpenAlex.

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39 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

12 authors at 2 institutions in 2 countries.

Hui PengNephrology Division, the Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Qianqian WangNephrology Division, the Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Tanqi LouNephrology Division, the Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Jun QinDepartment of Biochemistry and Molecular Biology, Baylor College of Medicine, Houston, TX, USA.
Sungyun JungDepartment of Biochemistry and Molecular Biology, Baylor College of Medicine, Houston, TX, USA.
Vivekananda ShettyThe Metabolomics and Proteomics Core, Baylor College of Medicine, Houston, TX, USA.
Feng LiThe Metabolomics and Proteomics Core, Baylor College of Medicine, Houston, TX, USA.
Yanlin WangNephrology Division, Department of Medicine, Baylor College of Medicine, Houston, TX, USA.
Xin-Hua FengDepartment of Surgery, Baylor College of Medicine, Houston, TX, USA.
William E MitchNephrology Division, Department of Medicine, Baylor College of Medicine, Houston, TX, USA.
Brett H GrahamDepartment of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX, USA.ORCID http://orcid.org/0000-0001-8451-8154
Zhaoyong HuNephrology Division, Department of Medicine, Baylor College of Medicine, Houston, TX, USA. zhaoyonh@bcm.edu.
Baylor College of Medicine · USSun Yat-sen University · CN

Funding

Cellular and Molecular Mechanisms of Renal FibrosisR01DK095835 · NIDDK · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI WANG, YANLIN · 2012 to 2021
$3.2M
Mechanisms of Protein-Energy-Wasting in Chronic Kidney DiseaseR01AR063686 · NIAMS · BAYLOR COLLEGE OF MEDICINE · PI HU, ZHAOYONG · 2013 to 2017
$1.7M
Targeting histone deacetylase 3 for chronic kidney diseaseI01BX002650 · VA · VA CONNECTICUT HEALTHCARE SYSTEM · PI YANLIN WANG · 2016 to 2026
–
BLRD VA I01 BX002650NIAMS NIH HHS R01 AR063686NIDDK NIH HHS R01 DK095835
6 · The paper itself

Abstract

Kidney injury initiates metabolic reprogramming in tubule cells that contributes to the development of chronic kidney disease (CKD). Exercise has been associated with beneficial effects in patients with CKD. Here we show that the induction of a myokine, irisin, improves kidney energy metabolism and prevents kidney damage. In response to kidney injury, mice with muscle-specific PGC-1α overexpression (mPGC-1α) exhibit reduced kidney damage and fibrosis. Metabolomics analysis reveals increased ATP production and improved energy metabolism in injured kidneys from mPGC-1α mice. We identify irisin as a serum factor that mediates these metabolic effects during progressive kidney injury by inhibiting TGF-β type 1 receptor. Irisin depletion from serum blunts the induction of oxygen consumption rate observed in tubule cells treated with mPGC-1α serum. In mice, recombinant irisin administration attenuates kidney damage and fibrosis and improves kidney functions. We suggest that myokine-mediated muscle-kidney crosstalk can suppress metabolic reprograming and fibrogenesis during kidney disease.

Indexed as

Adenosine TriphosphateAnimalsEnergy MetabolismFibronectinsFibrosisKidneyKidney TubulesMaleMetabolomicsMice, Inbred C57BLMice, TransgenicMuscle, SkeletalOxygen ConsumptionPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPhysical Conditioning, AnimalReceptors, Transforming Growth Factor betaAdenosine TriphosphateFibronectinsFNDC5 protein, mousePeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPpargc1a protein, mouseReceptors, Transforming Growth Factor betaRecombinant ProteinsTransforming Growth Factor beta1

Identifiers

PMID29138395
PMCPMC5686208
OpenAlexW2767932648

What OpenQuestion holds

Textmetadata
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.