Evidence map›Paper›PMID 26617693›Full record

ArticleInternational journal of clinical and experimental pathology2015

Intermedin attenuates myocardial infarction through activation of autophagy in a rat model of ischemic heart failure via both cAMP and MAPK/ERK1/2 pathways.

Peng Wei, Xiang-Jun Yang, Qiang Fu, Bing Han, Lin Ling, Jie Bai, Bin Zong, Chun-Ying Jiang

Open access · greenAbstract read
In one paragraph

Article in International journal of clinical and experimental pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

16 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Cardiovascular diagnosis and therapy · 2020
    Article
  7. Review
  8. Article
  9. Article
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  12. Review
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  15. Article
  16. The Effect of Wenxin Keli on the mRNA Expression Profile of Rabbits with Myocardial Infarction.Evidence-based complementary and alternative medicine : eCAM · 2016
    Article
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 3 institutions in 1 country.

Peng WeiDepartment of Cardiology, First Affiliated Hospital, Soochow University Suzhou 215006, China.
Xiang-Jun YangDepartment of Cardiology, First Affiliated Hospital, Soochow University Suzhou 215006, China.
Qiang FuDepartment of Cardiology, Xuzhou Central Hospital Xuzhou 221009, China.
Bing HanDepartment of Cardiology, Xuzhou Central Hospital Xuzhou 221009, China.
Lin LingDepartment of Cardiology, First Affiliated Hospital, Soochow University Suzhou 215006, China.
Jie BaiDepartment of Geriatrics Changhai Hospital of Second Military Medical University Shanghai 200433 China.
Bin ZongDepartment of Cardiology, Xuzhou Central Hospital Xuzhou 221009, China.
Chun-Ying JiangDepartment of Cardiology, Xuzhou Central Hospital Xuzhou 221009, China.
Xuzhou Central Hospital · CNSoochow University · CNSecond Military Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Intermedin is a proopiomelanocortin-derived peptide before opioid promoting cortical hormone, its main function embodies in mononuclear macrophages and neutrophilic granulocytes to inhibit the proinflammatory cytokines. The aim of this study is to determine intermedin attenuates myocardial infarction and its related mechanisms in a rat model of ischemic heart failure. After rat model of ischemic heart failure was set up, myocardial infarction, blood levels of activities of creatine kinase (CK), the MB isoenzyme of creatine kinase (CK-MB), lactate dehydrogenase (LDH) and cardiac troponin T (cTnT) were effectively reduced by treatment with intermedin. Tumor necrosis factor (TNF-α) and interleukin-6 (IL-6) in a rat model of ischemic heart failure were recovered by pretreatment with intermedin. Administrate of intermedin availably promoted cAMP contents and suppressed caspase-3 protein in ischemic heart failure rat. ERK1/2 and LC3 protein expression were significantly activated and autophagy was significantly promoted by intermedin in a rat model of ischemic heart failure. These results indicate that intermedin protected rat heart, attenuates myocardial infarction from ischemic heart failure in the rat model. The underlying mechanisms may include upregulation of cAMP, ERK1/2 and LC3 protein expression and activating of autophagy.

Indexed as

AdrenomedullinAnimalsAutophagyBlotting, WesternCyclic AMPDisease Models, AnimalEnzyme-Linked Immunosorbent AssayHeart FailureMAP Kinase Signaling SystemMitogen-Activated Protein Kinase KinasesMyocardial InfarctionNeuropeptidesRatsRats, Sprague-DawleyAdm2 protein, ratAdrenomedullinCyclic AMPMitogen-Activated Protein Kinase KinasesNeuropeptidesautophagycAMPERK1/2Intermedinischemic heart failure

Identifiers

PMID26617693
PMCPMC4637778
OpenAlexW2194859747

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.