Evidence map›Paper›PMID 29784903›Full record

ArticleScientific reports2018

Exercise ameliorates endoplasmic reticulum stress-mediated vascular dysfunction in mesenteric arteries in atherosclerosis.

Junyoung Hong, Kwangchan Kim, Eunkyung Park, Jonghae Lee, Melissa M Markofski, Sean P Marrelli, Yoonjung Park

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 21% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.

  1. Preclinical techniques to investigate exercise training in vascular pathophysiology.American journal of physiology. Heart and circulatory physiology · 2021
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  17. Exercise and Peripheral Arteriosclerosis.Advances in experimental medicine and biology · 2020
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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

7 authors at 2 institutions in 1 country.

Junyoung HongLaboratory of Integrated Physiology, Department of Health and Human Performance, University of Houston, Houston, TX, 77204, USA.
Kwangchan KimLaboratory of Integrated Physiology, Department of Health and Human Performance, University of Houston, Houston, TX, 77204, USA.
Eunkyung ParkLaboratory of Integrated Physiology, Department of Health and Human Performance, University of Houston, Houston, TX, 77204, USA.
Jonghae LeeLaboratory of Integrated Physiology, Department of Health and Human Performance, University of Houston, Houston, TX, 77204, USA.
Melissa M MarkofskiLaboratory of Integrated Physiology, Department of Health and Human Performance, University of Houston, Houston, TX, 77204, USA.
Sean P MarrelliDepartment of Neurology, McGovern Medical School at UT Health, Houston, TX, 77030, USA.
Yoonjung ParkLaboratory of Integrated Physiology, Department of Health and Human Performance, University of Houston, Houston, TX, 77204, USA. ypark10@uh.edu.ORCID 0000-0003-2257-8455
University of Houston · USThe University of Texas Health Science Center at Houston · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endoplasmic reticulum (ER) stress is closely associated with atherosclerosis, but the effects of exercise on ER stress-mediated endothelial dysfunction in atherosclerosis is not yet fully understood. We assessed endothelium-dependent vasodilation in isolated mesenteric arteries from wild type (WT), WT with exercise (WT-EX), ApoE knockout (ApoE KO), and ApoE KO mice with exercise (ApoE KO-EX). Vasodilation to acetylcholine (ACh) was elicited in the presence of inhibitors of ER stress, eNOS, caspase-1, and UCP-2 (Tudca, L-NAME, AC-YVARD-cmk, and Genipin, respectively) and the ER stress inducer (Tunicamycin). Immunofluorescence was used to visualize the expression of CHOP, as an indicator of ER stress, in superior mesenteric arteries (SMA). Dilation to ACh was attenuated in ApoE KO but was improved in ApoE KO-EX. Incubation of Tudca and AC-YVARD-cmk improved ACh-induced vasodilation in ApoE KO. L-NAME, tunicamycin, and Genipin attenuated vasodilation in WT, WT-EX and ApoE KO-EX, but not in ApoE KO. Exercise training reversed the increase in CHOP expression in the endothelium of SMA of ApoE KO mice. We conclude that ER stress plays a significant role in endothelial dysfunction of resistance arteries in atherosclerosis and that exercise attenuates ER stress and regulates its critical downstream signaling pathways including eNOS, UCP-2 and caspase-1.

Indexed as

Endoplasmic Reticulum StressPhysical Conditioning, AnimalAnimalsApolipoproteins EAtherosclerosisEndothelium, VascularInflammationMaleMesenteric ArteriesMiceMice, KnockoutOxidative StressVascular DiseasesVasodilationApolipoproteins E

Identifiers

PMID29784903
PMCPMC5962591
OpenAlexW2806863993

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.