Evidence map›Paper›PMID 29524006›Full record

ArticleBasic research in cardiology2018

Remote ischemic preconditioning fails to reduce infarct size in the Zucker fatty rat model of type-2 diabetes: role of defective humoral communication.

Joseph Wider, Vishnu V R Undyala, Peter Whittaker, James Woods, Xuequn Chen, Karin Przyklenk

Open access · greenAbstract read
In one paragraph

Article in Basic research in cardiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
6.0field-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, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.

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  10. Extracellular Vesicles and Ischemic Cardiovascular Diseases.Advances in experimental medicine and biology · 2023
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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

6 authors at 1 institution in 1 country.

Joseph WiderCardiovascular Research Institute, Wayne State University School of Medicine, Scott Hall, Room 4356, 540 E Canfield, Detroit, MI, 48201, USA.
Vishnu V R UndyalaCardiovascular Research Institute, Wayne State University School of Medicine, Scott Hall, Room 4356, 540 E Canfield, Detroit, MI, 48201, USA.
Peter WhittakerCardiovascular Research Institute, Wayne State University School of Medicine, Scott Hall, Room 4356, 540 E Canfield, Detroit, MI, 48201, USA.
James WoodsDepartment of Physiology, Wayne State University School of Medicine, Detroit, MI, USA.
Xuequn ChenDepartment of Physiology, Wayne State University School of Medicine, Detroit, MI, USA.
Karin PrzyklenkCardiovascular Research Institute, Wayne State University School of Medicine, Scott Hall, Room 4356, 540 E Canfield, Detroit, MI, 48201, USA. karinp@wayne.edu.ORCID 0000-0002-9602-6349
Wayne State University · US

Funding

Proinsulin ER Export and Beta Cell ER Homeostasis in Health and DiabetesR01DK110314 · NIDDK · WAYNE STATE UNIVERSITY · PI CHEN, XUEQUN · 2016 to 2021
$1.8M
Detroit Cardiovascular Training ProgramT32HL120822 · NHLBI · WAYNE STATE UNIVERSITY · PI LEVY, PHILLIP DAVID · 2014 to 2023
$1.8M
NHLBI NIH HHS NIH T32 HL120822-01NHLBI NIH HHS T32 HL120822NIDDK NIH HHS R01 DK110314
6 · The paper itself

Abstract

Remote ischemic preconditioning (RIPC), the phenomenon whereby brief ischemic episodes in distant tissues or organs render the heart resistant to infarction, has been exhaustively demonstrated in preclinical models. Moreover, emerging evidence suggests that exosomes play a requisite role in conveying the cardioprotective signal from remote tissue to the myocardium. However, in cohorts displaying clinically common comorbidities-in particular, type-2 diabetes-the infarct-sparing effect of RIPC may be confounded for as-yet unknown reasons. To investigate this issue, we used an integrated in vivo and in vitro approach to establish whether: (1) the efficacy of RIPC is maintained in the Zucker fatty rat model of type-2 diabetes, (2) the humoral transfer of cardioprotective triggers initiated by RIPC are transported via exosomes, and (3) diabetes is associated with alterations in exosome-mediated communication. We report that a standard RIPC stimulus (four 5-min episodes of hindlimb ischemia) reduced infarct size in normoglycemic Zucker lean rats, but failed to confer protection in diabetic Zucker fatty animals. Moreover, we provide novel evidence, via transfer of serum and serum fractions obtained following RIPC and applied to HL-1 cardiomyocytes subjected to hypoxia-reoxygenation, that diabetes was accompanied by impaired humoral communication of cardioprotective signals. Specifically, our data revealed that serum and exosome-rich serum fractions collected from normoglycemic rats attenuated hypoxia-reoxygenation-induced HL-1 cell death, while, in contrast, exosome-rich samples from Zucker fatty rats did not evoke protection in the HL-1 cell model. Finally, and unexpectedly, we found that exosome-depleted serum from Zucker fatty rats was cytotoxic and exacerbated hypoxia-reoxygenation-induced cardiomyocyte death.

Indexed as

Signal TransductionAnimalsCell DeathCell LineDiabetes Mellitus, Type 2Disease Models, AnimalExosomesHindlimbIschemic PreconditioningMaleMyocardial InfarctionMyocytes, CardiacRats, ZuckerRegional Blood FlowCardioprotectionExosomesExtracellular vesiclesInfarct sizeMass spectrometryMyocardial infarctionMyocardial ischemiaProteomicsRemote ischemic preconditioningType-2 diabetes

Identifiers

PMID29524006
PMCPMC6776086
OpenAlexW2792679487

What OpenQuestion holds

Textmetadata
LicenceTDM
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.