Evidence map›Paper›PMID 26259714›Full record

ArticleCardiovascular diabetology2015

Inhibition of DPP-4 reduces acute mortality after myocardial infarction with restoration of autophagic response in type 2 diabetic rats.

Hiromichi Murase, Atsushi Kuno, Takayuki Miki, Masaya Tanno, Toshiyuki Yano, Hidemichi Kouzu, Satoko Ishikawa, Toshiyuki Tobisawa, Makoto Ogasawara, Keitaro Nishizawa and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cardiovascular diabetology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
5.5field-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

29 citing papers in PubMed, 57 citations in OpenAlex.

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  3. Role of AMP deaminase in diabetic cardiomyopathy.Molecular and cellular biochemistry · 2024
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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

11 authors at 1 institution in 1 country.

Hiromichi MuraseDepartment of Cardiovascular, Renal and Metabolic Medicine, Sapporo Medical University School of Medicine, South-1, West-16, Chuo-ku, Sapporo, 060-8543, Japan. michi_seramu_9754@yahoo.co.jp.
Atsushi KunoDepartment of Cardiovascular, Renal and Metabolic Medicine, Sapporo Medical University School of Medicine, South-1, West-16, Chuo-ku, Sapporo, 060-8543, Japan. kuno@sapmed.ac.jp.
Takayuki MikiDepartment of Cardiovascular, Renal and Metabolic Medicine, Sapporo Medical University School of Medicine, South-1, West-16, Chuo-ku, Sapporo, 060-8543, Japan. tmiki@sapmed.ac.jp.
Masaya TannoDepartment of Cardiovascular, Renal and Metabolic Medicine, Sapporo Medical University School of Medicine, South-1, West-16, Chuo-ku, Sapporo, 060-8543, Japan. tannnom@sapmed.ac.jp.
Toshiyuki YanoDepartment of Cardiovascular, Renal and Metabolic Medicine, Sapporo Medical University School of Medicine, South-1, West-16, Chuo-ku, Sapporo, 060-8543, Japan. tyano@sapmed.ac.jp.
Hidemichi KouzuDepartment of Cardiovascular, Renal and Metabolic Medicine, Sapporo Medical University School of Medicine, South-1, West-16, Chuo-ku, Sapporo, 060-8543, Japan. kouzu@sapmed.ac.jp.
Satoko IshikawaDepartment of Cardiovascular, Renal and Metabolic Medicine, Sapporo Medical University School of Medicine, South-1, West-16, Chuo-ku, Sapporo, 060-8543, Japan. ishikawas@sapmed.ac.jp.
Toshiyuki TobisawaDepartment of Cardiovascular, Renal and Metabolic Medicine, Sapporo Medical University School of Medicine, South-1, West-16, Chuo-ku, Sapporo, 060-8543, Japan. tobisawadesu@yahoo.co.jp.
Makoto OgasawaraDepartment of Cardiovascular, Renal and Metabolic Medicine, Sapporo Medical University School of Medicine, South-1, West-16, Chuo-ku, Sapporo, 060-8543, Japan. ogasawara13202831@yahoo.co.jp.
Keitaro NishizawaDepartment of Cardiovascular, Renal and Metabolic Medicine, Sapporo Medical University School of Medicine, South-1, West-16, Chuo-ku, Sapporo, 060-8543, Japan. nishizawa_1114@sapmed.ac.jp.
Tetsuji MiuraDepartment of Cardiovascular, Renal and Metabolic Medicine, Sapporo Medical University School of Medicine, South-1, West-16, Chuo-ku, Sapporo, 060-8543, Japan. miura@sapmed.ac.jp.
Sapporo Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundType 2 diabetes mellitus (T2DM) worsens the outcome after myocardial infarction (MI). Here, we hypothesized that inhibition of dipeptidyl peptidase-4 (DPP-4) improves survival after MI in T2DM by modifying autophagy in the non-infarcted region of the heart. METHODS AND

resultsUnder baseline conditions, there was no significant difference between levels of myocardial autophagy marker proteins in OLETF, a rat model of T2DM, and in LETO, a non-diabetic control. However, in contrast to the response in LETO, LC3-II protein and LC3-positive autophagosomes in the non-infarcted region of the myocardium were not increased after MI in OLETF. The altered autophagic response in OLETF was associated with lack of AMPK/ULK-1 activation, attenuated response of Akt/mTOR/S6 signaling and increased Beclin-1-Bcl-2 interaction after MI. Treatment with vildagliptin (10 mg/kg/day s.c.), a DPP-4 inhibitor, suppressed Beclin-1-Bcl-2 interaction and increased both LC3-II protein level and autophagosomes in the non-infarcted region in OLETF, though it did not normalize AMPK/ULK-1 or mTOR/S6 signaling. Plasma insulin level, but not glucose level, was significantly reduced by vildagliptin at the dose used in this study. Survival rate at 48 h after MI was significantly lower in OLETF than in LETO (32 vs. 82%), despite similar infarct sizes. Vildagliptin improved the survival rate in OLETF to 80%, the benefit of which was abrogated by chloroquine, an autophagy inhibitor.

conclusionsThe results indicate that vildagliptin reduces T2DM-induced increase in post-MI acute mortality possibly by restoring the autophagic response through attenuation of Bcl-2-Beclin-1 interaction.

Indexed as

AdamantaneAnimalsApoptosis Regulatory ProteinsAutophagyBeclin-1ChloroquineDiabetes Mellitus, Type 2Dipeptidyl Peptidase 4Dipeptidyl-Peptidase IV InhibitorsDisease Models, AnimalDrug Administration ScheduleInjections, SubcutaneousMaleMicrotubule-Associated ProteinsMyocardial InfarctionMyocardiumAdamantaneAnxa3 protein, ratApoptosis Regulatory ProteinsBeclin-1Becn1 protein, ratChloroquineDipeptidyl Peptidase 4Dipeptidyl-Peptidase IV InhibitorsDPP4 protein, ratMicrotubule-Associated ProteinsNitrilesProto-Oncogene Proteins c-bcl-2PyrrolidinesVildagliptin

Identifiers

PMID26259714
PMCPMC4531441
OpenAlexW1914678473

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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.