Evidence map›Paper›PMID 33469904›Full record

ArticleThrombosis and haemostasis2021

Endothelial β1 Integrin-Mediated Adaptation to Myocardial Ischemia.

Carina Henning, Anna Branopolski, Paula Follert, Oksana Lewandowska, Aysel Ayhan, Marcel Benkhoff, Ulrich Flögel, Malte Kelm, Christian Heiss, Eckhard Lammert

Open access · hybridAbstract readVideo-Audio Media
In one paragraph

Article in Thrombosis and haemostasis, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

11 citing papers in PubMed, 20 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

10 authors at 4 institutions in 2 countries.

Carina Henning *Institute of Metabolic Physiology, Department of Biology, Heinrich-Heine-University, Düsseldorf, Germany.
Anna Branopolski *Institute of Metabolic Physiology, Department of Biology, Heinrich-Heine-University, Düsseldorf, Germany.
Paula FollertInstitute of Metabolic Physiology, Department of Biology, Heinrich-Heine-University, Düsseldorf, Germany.
Oksana LewandowskaInstitute of Metabolic Physiology, Department of Biology, Heinrich-Heine-University, Düsseldorf, Germany.
Aysel AyhanDivision of Cardiology, Pulmonology, and Vascular Medicine, Heinrich-Heine-University, Düsseldorf, Germany.
Marcel BenkhoffDivision of Cardiology, Pulmonology, and Vascular Medicine, Heinrich-Heine-University, Düsseldorf, Germany.
Ulrich FlögelInstitute for Molecular Cardiology, University Hospital Düsseldorf, Heinrich-Heine-University, Düsseldorf, Germany.
Malte KelmDivision of Cardiology, Pulmonology, and Vascular Medicine, Heinrich-Heine-University, Düsseldorf, Germany.
Christian HeissDivision of Cardiology, Pulmonology, and Vascular Medicine, Heinrich-Heine-University, Düsseldorf, Germany.ORCID 0000-0002-3212-8995
Eckhard LammertInstitute of Metabolic Physiology, Department of Biology, Heinrich-Heine-University, Düsseldorf, Germany.
Heinrich Heine University Düsseldorf · DEDeutsches Diabetes-Zentrum e.V. · DEDüsseldorf University Hospital · DEUniversity of Surrey · GB

Funding

SFB 1116 Deutsche Forschungsgemeinschaft (DFG)SFB 974 Deutsche Forschungsgemeinschaft (DFG)
6 · The paper itself

Abstract

backgroundShort episodes of myocardial ischemia can protect from myocardial infarction. However, the role of endothelial β1 integrin in these cardioprotective ischemic events is largely unknown.

objectiveIn this study we investigated whether endothelial β1 integrin is required for cardiac adaptation to ischemia and protection from myocardial infarction.

methodsHere we introduced transient and permanent left anterior descending artery (LAD) occlusions in mice. We inhibited β1 integrin by intravenous injection of function-blocking antibodies and tamoxifen-induced endothelial cell (EC)-specific deletion of

resultsTransient LAD occlusions were found to increase EC proliferation and arteriole formation in the entire myocardium. These effects required β1 integrin on ECs, except for arteriole formation in the ischemic part of the myocardium. Furthermore, this integrin subunit was also relevant for basal and mechanically induced proliferation of human coronary artery ECs. Notably, β1 integrin was needed for cardioprotection induced by transient LAD occlusions, and the absence of endothelial β1 integrin resulted in impaired growth of blood vessels into the infarcted myocardium and reduced cardiac function after permanent LAD occlusion.

conclusionWe showed that endothelial β1 integrin is required for adaptation of the heart to cardiac ischemia and protection from myocardial infarction.

Indexed as

Ischemic Preconditioning, MyocardialAnimalsCell ProliferationCoronary VesselsDisease Models, AnimalEndothelial CellsHumansIntegrin beta1MaleMiceMice, Inbred C57BLMice, KnockoutMyocardial InfarctionNeovascularization, PhysiologicNitric Oxide Synthase Type IIISignal TransductionIntegrin beta1Itgb1 protein, humanItgb1 protein, mouseNitric Oxide Synthase Type IIINos3 protein, mouse

Identifiers

PMID33469904
PMCPMC8180378
OpenAlexW3119922456

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.