Evidence map›Paper›PMID 31061533›Full record

ArticleActa pharmacologica Sinica2019

Irisin exerts a therapeutic effect against myocardial infarction via promoting angiogenesis.

Qiao Liao, Shuang Qu, Lu-Xun Tang, Liang-Peng Li, Duo-Fen He, Chun-Yu Zeng, Wei Eric Wang

Open access · bronzeAbstract read
In one paragraph

Article in Acta pharmacologica Sinica, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed, 1 pooled it
5.7field-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

56 citing papers in PubMed, 1 synthesis or guideline pooled it, 81 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.

Qiao LiaoDepartment of Cardiology, Daping Hospital, Third Military Medical University, Chongqing, 400042, China.
Shuang QuDepartment of Cardiology, Daping Hospital, Third Military Medical University, Chongqing, 400042, China.
Lu-Xun TangDepartment of Cardiology, Daping Hospital, Third Military Medical University, Chongqing, 400042, China.
Liang-Peng LiDepartment of Cardiology, Daping Hospital, Third Military Medical University, Chongqing, 400042, China.
Duo-Fen HeDepartment of Cardiology, Daping Hospital, Third Military Medical University, Chongqing, 400042, China.
Chun-Yu ZengDepartment of Cardiology, Daping Hospital, Third Military Medical University, Chongqing, 400042, China. chunyuzeng01@163.com.
Wei Eric WangDepartment of Cardiology, Daping Hospital, Third Military Medical University, Chongqing, 400042, China. weiericwang@163.com.
Army Medical University · CNChongqing University · CNDaping Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Irisin, a myokine, is cleaved from the extracellular portion of fibronectin domain-containing 5 protein in skeletal muscle and myocardium and secreted into circulation as a hormone during exercise. Irisin has been found to exert protective effects against lung and heart injuries. However, whether irisin influences myocardial infarction (MI) remains unclear. In this study we investigated the therapeutic effects of irisin in an acute MI model and its underlying mechanisms. Adult C57BL/6 mice were subjected to ligation of the left anterior descending coronary artery and treated with irisin for 2 weeks after MI. Cardiac function was assessed using echocardiography. We found that irisin administration significantly alleviated MI-induced cardiac dysfunction and ventricular dilation at 4 weeks post-MI. Irisin significantly reduced infarct size and fibrosis in post-MI hearts. Irisin administration significantly increased angiogenesis in the infarct border zone and decreased cardiomyocyte apoptosis, but did not influence cardiomyocyte proliferation. In human umbilical vein endothelial cells (HUVEC), irisin significantly increased the phosphorylation of ERK, and promoted the migration of HUVEC detected in wound-healing and transwell chamber migration assay. The effects of irisin were blocked by the ERK inhibitor U0126. In conclusion, irisin improves cardiac function and reduces infarct size in post-MI mouse heart. The therapeutic effect is associated with its pro-angiogenic function through activating ERK signaling pathway.

Indexed as

AnimalsApoptosisButadienesCell MovementDisease Models, AnimalFibronectinsHumansHuman Umbilical Vein Endothelial CellsMaleMiceMice, Inbred C57BLMyocardial InfarctionNeovascularization, PathologicNitrilesRecombinant ProteinsButadienesFibronectinsFNDC5 protein, mouseNitrilesRecombinant ProteinsU 0126angiogenesisERK signal pathwayirisinmyocardial infarctionU0126

Identifiers

PMID31061533
PMCPMC6786355
OpenAlexW2944766178

What OpenQuestion holds

Textmetadata
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.