Evidence map›Paper›PMID 31388770›Full record

ArticleBasic research in cardiology2019

DPP-4 inhibition by linagliptin prevents cardiac dysfunction and inflammation by targeting the Nlrp3/ASC inflammasome.

Yochai Birnbaum, Dat Tran, Mandeep Bajaj, Yumei Ye

Abstract read
PubMed Publisher
In one paragraph

Article in Basic research in cardiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 2 pooled it
6.6field-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

39 citing papers in PubMed, 2 syntheses or guidelines pooled it, 67 citations in OpenAlex.

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  20. Guidelines on models of diabetic heart disease.American journal of physiology. Heart and circulatory physiology · 2022
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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

4 authors at 2 institutions in 1 country.

Yochai BirnbaumSection of Cardiology, Baylor College of Medicine, and the Texas Heart Institute, Baylor St Luke Medical Center, Houston, TX, USA. ybirnbau@bcm.edu.ORCID http://orcid.org/0000-0001-7653-6328
Dat TranSchool of Medicine, University of Texas Medical Branch, Galveston, TX, USA.
Mandeep BajajSection of Endocrinology, Baylor College of Medicine, Houston, TX, USA.
Yumei YeThe Department of Biochemistry and Molecular Biology, University of Texas Medical Branch, Galveston, TX, USA.
Baylor College of Medicine · USThe University of Texas Medical Branch at Galveston · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We compared the effects of linagliptin (Lina, a DPP4 inhibitor) and GLP-1 receptor activation by exenatide followed by exendin-4 in an infusion pump (EX) on infarct size (IS), post-infarction activation of the inflammasome and remodeling in wild-type (WT) and db/db diabetic mice. Mice underwent 30 min ischemia followed by 24 h reperfusion. IS was assessed by TTC. Additional mice underwent permanent coronary artery occlusion. Echocardiography was performed 2w after infarction. Activation of the inflammasome in the border zone of the infarction was assessed by rt-PCR and ELISA 2w after reperfusion. Further in vitro experiments were done using primary human cardiofibroblasts and cardiomyocytes exposed to simulated ischemia-reoxygenation. Lina and EX limited IS in both the WT and the db/db mice. Lina and EX equally improved ejection fraction in both the WT and the db/db mice. mRNA levels of ASC, NALP3, IL-1β, IL-6, Collagen-1, and Collagen-3 were higher in the db/db mice than in the WT mice. Infarction increased these levels in the WT and db/db mice. Lina more than EX attenuated the increase in ASC, NALP3, IL-1β, IL-6, Collagen-1 and Collagen-3, TNFα and IL-1β, and decreased apoptosis, especially in the db/db mice. In vitro experiments showed that Lina, but not EX, attenuated the increase in TLR4 expression, an effect that was dependent on p38 activation with downstream upregulation of Let-7i and miR-146b levels. Lina and EX had similar effects on IS and post-infarction function, but Lina attenuated the activation of the inflammasome and the upregulation of collagen-1 and collagen-3 more than direct GLP-1 receptor activation. This effect depends on p38 activation with downstream upregulation of miR-146b levels that suppresses TLR4 expression.

Indexed as

Diabetes Mellitus, Type 2AnimalsDiabetes Mellitus, ExperimentalDiabetic CardiomyopathiesDipeptidyl Peptidase 4Dipeptidyl-Peptidase IV InhibitorsInflammasomesLinagliptinMiceMice, Inbred C57BLMyocardial InfarctionNLR Family, Pyrin Domain-Containing 3 ProteinSignal TransductionDipeptidyl Peptidase 4Dipeptidyl-Peptidase IV InhibitorsDpp4 protein, mouseInflammasomesLinagliptinNLR Family, Pyrin Domain-Containing 3 ProteinDPP4 inhibitorGLP-1microRNAMyocardial infarctionNlrp3/ASC inflammasomeTLR4

Identifiers

PMID31388770
OpenAlexW2966692841

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.