Evidence map›Paper›PMID 26305684›Full record

ArticlePloS one2015

Irisin Controls Growth, Intracellular Ca2+ Signals, and Mitochondrial Thermogenesis in Cardiomyoblasts.

Chao Xie, Yuan Zhang, Tran D N Tran, Hai Wang, Shiwu Li, Eva Vertes George, Haoyang Zhuang, Peilan Zhang, Avi Kandel, Yimu Lai and 5 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

37 citing papers in PubMed, 101 citations in OpenAlex.

  1. Myokines and mitochondrial function in cardiometabolic diseases.Journal of physiology and biochemistry · 2026
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  17. Antioxidant Effects of Irisin in Liver Diseases: Mechanistic Insights.Oxidative medicine and cellular longevity · 2022
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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

15 authors at 5 institutions in 2 countries.

Chao XieDepartment of Pathology, Immunology, and Laboratory Medicine, University of Florida College of Medicine, Gainesville, FL, 32610, United States of America.
Yuan ZhangDepartment of Pathology, Immunology, and Laboratory Medicine, University of Florida College of Medicine, Gainesville, FL, 32610, United States of America; Center for Stem Cell & Regenerative Medicine, The Second Hospital of Shandong University, Jinan, 250012, P. R. China.
Tran D N TranDepartment of Comparative Biomedical Sciences, School of Veterinary Medicine, Louisiana State University, Baton Rouge, LA, 70803, United States of America.
Hai WangDepartment of Pathology, Immunology, and Laboratory Medicine, University of Florida College of Medicine, Gainesville, FL, 32610, United States of America.
Shiwu LiDepartment of Pathology, Immunology, and Laboratory Medicine, University of Florida College of Medicine, Gainesville, FL, 32610, United States of America.
Eva Vertes GeorgeDepartment of Pathology, Immunology, and Laboratory Medicine, University of Florida College of Medicine, Gainesville, FL, 32610, United States of America.
Haoyang ZhuangDepartment of Medicine, University of Florida College of Medicine, Gainesville, FL, 32610, United States of America.
Peilan ZhangDepartment of Medicinal Chemistry, Center for Natural Products, Drug Discovery and Development, College of Pharmacy, University of Florida, Gainesville, FL, 32610, United States of America.
Avi KandelDepartment of Pathology, Immunology, and Laboratory Medicine, University of Florida College of Medicine, Gainesville, FL, 32610, United States of America.
Yimu LaiDepartment of Cell Biology and Anatomy, University of South Carolina of Medicine, Columbia, SC, 29209, United States of America.
Dongqi TangCenter for Stem Cell & Regenerative Medicine, The Second Hospital of Shandong University, Jinan, 250012, P. R. China.
Westley H ReevesDepartment of Medicine, University of Florida College of Medicine, Gainesville, FL, 32610, United States of America.
Henrique ChengDepartment of Comparative Biomedical Sciences, School of Veterinary Medicine, Louisiana State University, Baton Rouge, LA, 70803, United States of America.
Yousong DingDepartment of Medicinal Chemistry, Center for Natural Products, Drug Discovery and Development, College of Pharmacy, University of Florida, Gainesville, FL, 32610, United States of America.
Li-Jun YangDepartment of Pathology, Immunology, and Laboratory Medicine, University of Florida College of Medicine, Gainesville, FL, 32610, United States of America.
University of Florida · USFlorida College · USLouisiana State University · USSecond Hospital of Shandong University · CNUniversity of South Carolina · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Exercise offers short-term and long-term health benefits, including an increased metabolic rate and energy expenditure in myocardium. The newly-discovered exercise-induced myokine, irisin, stimulates conversion of white into brown adipocytes as well as increased mitochondrial biogenesis and energy expenditure. Remarkably, irisin is highly expressed in myocardium, but its physiological effects in the heart are unknown. The objective of this work is to investigate irisin's potential multifaceted effects on cardiomyoblasts and myocardium. For this purpose, H9C2 cells were treated with recombinant irisin produced in yeast cells (r-irisin) and in HEK293 cells (hr-irisin) for examining its effects on cell proliferation by MTT [3-(4, 5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] assay and on gene transcription profiles by qRT-PCR. R-irisin and hr-irisin both inhibited cell proliferation and activated genes related to cardiomyocyte metabolic function and differentiation, including myocardin, follistatin, smooth muscle actin, and nuclear respiratory factor-1. Signal transduction pathways affected by r-irisin in H9C2 cells and C57BL/6 mice were examined by detecting phosphorylation of PI3K-AKT, p38, ERK or STAT3. We also measured intracellular Ca2+ signaling and mitochondrial thermogenesis and energy expenditure in r-irisin-treated H9C2 cells. The results showed that r-irisin, in a certain concentration rage, could activate PI3K-AKT and intracellular Ca2+ signaling and increase cellular oxygen consumption in H9C2 cells. Our study also suggests the existence of irisin-specific receptor on the membrane of H9C2 cells. In conclusion, irisin in a certain concentration rage increased myocardial cell metabolism, inhibited cell proliferation and promoted cell differentiation. These effects might be mediated through PI3K-AKT and Ca2+ signaling, which are known to activate expression of exercise-related genes such as follistatin and myocardin. This work supports the value of exercise, which promotes irisin release.

Indexed as

AnimalsCalcium SignalingCell DifferentiationCell ProliferationEnergy MetabolismFibronectinsGene Expression RegulationHEK293 CellsHumansMiceMitochondriaMyoblasts, CardiacMyocardiumThermogenesisFibronectinsFNDC5 protein, mouse

Identifiers

PMID26305684
PMCPMC4549318
OpenAlexW1886130798

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.