Evidence map›Paper›PMID 30993599›Full record

ArticleCell stress & chaperones2019

Irisin ameliorates septic cardiomyopathy via inhibiting DRP1-related mitochondrial fission and normalizing the JNK-LATS2 signaling pathway.

Ying Tan, Haichun Ouyang, Xiaochan Xiao, Jiankai Zhong, Maolong Dong

Open access · bronzeAbstract read
In one paragraph

Article in Cell stress & chaperones, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
2.5field-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

43 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 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

5 authors at 3 institutions in 1 country.

Ying TanDepartment of Emergency Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China.
Haichun OuyangDepartment of Cardiology, Shunde Hospital, Southern Medical University, Foshan, 528300, Guangdong, China.
Xiaochan XiaoDepartment of Emergency Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China.
Jiankai ZhongDepartment of Cardiology, Shunde Hospital, Southern Medical University, Foshan, 528300, Guangdong, China. doctor-zh@qq.com.
Maolong DongDepartment of Emergency Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China. 2206723777@qq.com.
Southern Medical University · CNNanfang Hospital · CNThe First People's Hospital of Shunde · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Irisin plays a protective effect in acute and chronic myocardial damage, but its role in septic cardiomyopathy is unclear. The aim of our study was to explore the in vivo and in vitro effects of irisin using an LPS-induced septic cardiomyopathy model. Our results demonstrated that irisin treatment attenuated LPS-mediated cardiomyocyte death and myocardial dysfunction. At the molecular level, LPS application was associated with mitochondrial oxidative injury, cardiomyocyte ATP depletion and caspase-related apoptosis activation. In contrast, the irisin treatment sustained mitochondrial function by inhibiting DRP1-related mitochondrial fission and the reactivation of mitochondrial fission impaired the protective action of irisin on inflammation-attacked mitochondria and cardiomyocytes. Additionally, we found that irisin modulated DRP1-related mitochondrial fission through the JNK-LATS2 signaling pathway. JNK activation and/or LATS2 overexpression abolished the beneficial effects of irisin on LPS-mediated mitochondrial stress and cardiomyocyte death. Altogether, our results illustrate that LPS-mediated activation of DRP1-related mitochondrial fission through the JNK-LATS2 pathway participates in the pathogenesis of septic cardiomyopathy. Irisin could be used in the future as an effective therapy for sepsis-induced myocardial depression because it corrects DRP1-related mitochondrial fission and normalizes the JNK-LATS2 signaling pathway.

Indexed as

AnimalsCardiomyopathiesDynaminsFibronectinsLipopolysaccharidesMAP Kinase Signaling SystemMice, Inbred C57BLMitochondriaMitochondrial DynamicsMyocytes, CardiacDnm1l protein, mouseDynaminsFibronectinsFNDC5 protein, mouseLipopolysaccharidesDRP1-related mitochondrial fissionIrisinJNK-LATS2 signaling pathway

Identifiers

PMID30993599
PMCPMC6527615
OpenAlexW2939573775

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.