Evidence map›Paper›PMID 25752217›Full record

ArticleJournal of cellular and molecular medicine2015

Oncostatin M (OSM) protects against cardiac ischaemia/reperfusion injury in diabetic mice by regulating apoptosis, mitochondrial biogenesis and insulin sensitivity.

Dongdong Sun, Shuang Li, Hao Wu, Mingming Zhang, Xiaotian Zhang, Liping Wei, Xing Qin, Erhe Gao

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

31 citing papers in PubMed, 59 citations in OpenAlex.

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  15. The Key Role of IPMolecules (Basel, Switzerland) · 2020
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  16. The Effects ofNutrients · 2020
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  17. Review
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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

8 authors at 4 institutions in 2 countries.

Dongdong SunDepartment of Cardiology, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
Shuang LiDepartment of Cardiology, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
Hao WuDepartment of Toxicology, School of Public Health, Fourth Military Medical University, Xi'an, China.
Mingming ZhangDepartment of Cardiology, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
Xiaotian ZhangDepartment of Cardiology, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
Liping WeiDepartment of Cardiology, Tianjin Union Medicine Center, Tianjin, China.
Xing QinDepartment of Cardiology, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
Erhe GaoCenter for Translational Medicine, Temple University School of Medicine, Philadelphia, PA, USA.
Air Force Medical University · CNXijing Hospital · CNTemple University · USUnion Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oncostatin M (OSM) exhibits many unique biological activities by activating Oβ receptor. However, its role in myocardial I/R injury in diabetic mice remains unknown. The involvement of OSM was assessed in diabetic mice which underwent myocardial I/R injury by OSM treatment or genetic deficiency of OSM receptor Oβ. Its mechanism on cardiomyocyte apoptosis, mitochondrial biogenesis and insulin sensitivity were further studied. OSM alleviated cardiac I/R injury by inhibiting cardiomyocyte apoptosis through inhibition of inositol pyrophosphate 7 (IP7) production, thus activating PI3K/Akt/BAD pathway, decreasing Bax expression while up-regulating Bcl-2 expression and decreasing the ratio of Bax to Bcl-2 in db/db mice. OSM enhanced mitochondrial biogenesis and mitochondrial function in db/db mice subjected to cardiac I/R injury. On the contrary, OSM receptor Oβ knockout exacerbated cardiac I/R injury, increased IP7 production, enhanced cardiomyocyte apoptosis, impaired mitochondrial biogenesis, glucose homoeostasis and insulin sensitivity in cardiac I/R injured diabetic mice. Inhibition of IP7 production by TNP (IP6K inhibitor) exerted similar effects of OSM. The mechanism of OSM on cardiac I/R injury in diabetic mice is partly associated with IP7/Akt and adenine mononucleotide protein kinase/PGC-1α pathway. OSM protects against cardiac I/R Injury by regulating apoptosis, insulin sensitivity and mitochondrial biogenesis in diabetic mice through inhibition of IP7 production.

Indexed as

Insulin ResistanceAnimalsApoptosisBlotting, WesternDiabetes Mellitus, ExperimentalGlucoseHomeostasisInositol PhosphatesMice, 129 StrainMice, KnockoutMice, Mutant StrainsMyocardial Reperfusion InjuryMyocardiumOncostatin MOrganelle BiogenesisProtective AgentsGlucoseInositol PhosphatesOncostatin MProtective AgentsReceptors, Oncostatin Mdiabetesinositol pyrophosphate 7ischaemia/Reperfusion injuryoncostatin M

Identifiers

PMID25752217
PMCPMC4459845
OpenAlexW2002557217

What OpenQuestion holds

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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.