Evidence map›Paper›PMID 28840975›Full record

ArticleJournal of cellular and molecular medicine2018

Cardioprotection mediated by exosomes is impaired in the setting of type II diabetes but can be rescued by the use of non-diabetic exosomes in vitro.

Sean M Davidson, Jaime A Riquelme, Kaloyan Takov, Jose M Vicencio, Claire Boi-Doku, Vanessa Khoo, Christian Doreth, Dina Radenkovic, Sergio Lavandero, Derek M Yellon

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed, 2 pooled it
5.1field-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

74 citing papers in PubMed, 2 syntheses or guidelines pooled it, 103 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Extracellular vesicle-mediated mechanisms and therapeutic potential in acute lung injury.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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14 more citing papers are in PubMed but not listed here.

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 2 institutions in 2 countries.

Sean M DavidsonThe Hatter Cardiovascular Institute, University College London, London, UK.ORCID 0000-0001-5182-4980
Jaime A RiquelmeThe Hatter Cardiovascular Institute, University College London, London, UK.
Kaloyan TakovThe Hatter Cardiovascular Institute, University College London, London, UK.
Jose M VicencioCancer Institute, University College London, London, UK.
Claire Boi-DokuThe Hatter Cardiovascular Institute, University College London, London, UK.
Vanessa KhooThe Hatter Cardiovascular Institute, University College London, London, UK.
Christian DorethThe Hatter Cardiovascular Institute, University College London, London, UK.
Dina RadenkovicThe Hatter Cardiovascular Institute, University College London, London, UK.
Sergio LavanderoAdvanced Center for Chronic Disease (ACCDiS), Facultad de Ciencias Químicas y Farmacéuticas & Facultad de Medicina, Universidad de Chile, Santiago, Chile.
Derek M YellonThe Hatter Cardiovascular Institute, University College London, London, UK.
University College London · GBAdvanced Center for Chronic Diseases · CL

Funding

Medical Research Council MR/K002066/1
6 · The paper itself

Abstract

Many patients with ischaemic heart disease also have diabetes. As myocardial infarction is a major cause of mortality and morbidity in these patients, treatments that increase cell survival in response to ischaemia and reperfusion are needed. Exosomes-nano-sized, lipid vesicles released from cells-can protect the hearts of non-diabetic rats. We previously showed that exosomal HSP70 activates a cardioprotective signalling pathway in cardiomyocytes culminating in ERK1/2 and HSP27 phosphorylation. Here, we investigated whether the exosomal cardioprotective pathway remains intact in the setting of type II diabetes. Exosomes were isolated by differential centrifugation from non-diabetic and type II diabetic patients, from non-diabetic and Goto Kakizaki type II diabetic rats, and from normoglycaemic and hyperglycaemic endothelial cells. Exosome size and number were not significantly altered by diabetes. CD81 and HSP70 exosome markers were increased in diabetic rat exosomes. However, exosomes from diabetic rats no longer activated the ERK1/2 and HSP27 cardioprotective pathway and were no longer protective in a primary rat cardiomyocytes model of hypoxia and reoxygenation injury. Hyperglycaemic culture conditions were sufficient to impair protection by endothelial exosomes. Importantly, however, exosomes from non-diabetic rats retained the ability to protect cardiomyocytes from diabetic rats. Exosomes from diabetic plasma have lost the ability to protect cardiomyocytes, but protection can be restored with exosomes from non-diabetic plasma. These results support the concept that exosomes may be used to protect cardiomyocytes against ischaemia and reperfusion injury, even in the setting of type II diabetes.

Indexed as

AgedAged, 80 and overAnimalsCardiotonic AgentsDiabetes Mellitus, Type 2ExosomesExtracellular Signal-Regulated MAP KinasesHSP27 Heat-Shock ProteinsHSP70 Heat-Shock ProteinsHumansHuman Umbilical Vein Endothelial CellsMaleMiddle AgedMyocytes, CardiacNanoparticlesPhosphorylationCardiotonic AgentsExtracellular Signal-Regulated MAP KinasesHSP27 Heat-Shock ProteinsHSP70 Heat-Shock ProteinsTetraspanin 28cardioprotectiondiabetesExosomesischaemiareperfusion

Identifiers

PMID28840975
PMCPMC5742744
OpenAlexW2746108841

What OpenQuestion holds

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LicenceCC BY
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.