Evidence map›Paper›PMID 18063803›Full record

ReviewJournal of applied physiology (Bethesda, Md. : 1985)2008

Importance of hemodynamic forces as signals for exercise-induced changes in endothelial cell phenotype.

M Harold Laughlin, Sean C Newcomer, Shawn B Bender

Abstract readReview
In one paragraph

Review in Journal of applied physiology (Bethesda, Md. : 1985), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 162 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
162citing papers in PubMed, 4 pooled it
9.1field-weighted citation impact, top 2% 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

162 citing papers in PubMed, 4 syntheses or guidelines pooled it, 320 citations in OpenAlex.

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  6. Stent edge vascular response and in-stent geometry after aerobic exercise.Cardiovascular intervention and therapeutics · 2021
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  19. Exercise-induced brachial artery vasodilation: effects of antioxidants and exercise training in elderly men.American journal of physiology. Heart and circulatory physiology · 2010
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102 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

3 authors at 1 institution in 1 country.

M Harold LaughlinDepartment of Biomedical Sciences, College of Veterinary Medicine, 1600 E. Rollins Rd., University of Missouri, Columbia, MO 65211, USA. laughlinm@missouri.edu
Sean C Newcomer
Shawn B Bender
University of Missouri · US

Funding

Vascular Biology: Exercise Training and Vascular DiseaseP01HL052490 · NHLBI · UNIVERSITY OF MISSOURI-COLUMBIA · PI LAUGHLIN, M HAROLD · 1995 to 2010
$19.3M
TRAINING: MUSCLE BLOOD FLOW &CAPILLARY DYNAMICSR01HL036088 · NHLBI · UNIVERSITY OF MISSOURI-COLUMBIA · PI LAUGHLIN, M HAROLD · 1985 to 2013
$4.0M
eNOS: Metabolism &Vascular Biology in Health &DiseaseR24RR018276 · NCRR · UNIVERSITY OF MISSOURI-COLUMBIA · PI LAUGHLIN, M HAROLD · 2003 to 2007
$3.3M
Exercise &Health: Integration from Molecule to PatientT32AR048523 · NIAMS · UNIVERSITY OF MISSOURI-COLUMBIA · PI TERJUNG, RONALD L · 2003 to 2013
$2.5M
NCRR NIH HHS R24 RR018276NCRR NIH HHS RR-18276NHLBI NIH HHS HL-36088NHLBI NIH HHS HL-52490NHLBI NIH HHS P01 HL052490NHLBI NIH HHS R01 HL036088NIAMS NIH HHS AR-048523NIAMS NIH HHS T32 AR048523
6 · The paper itself

Abstract

Current evidence indicates that the ability of physical activity to sustain a normal phenotype of arterial endothelial cells (ECs) plays a central role in the beneficial effects of exercise (Ex) on atherosclerotic disease. Here we evaluate the strength of evidence that shear stress (SS) and/or circumferential wall stress (stretch) are the primary signals, produced by bouts of Ex, that signal altered gene expression in arterial ECs, thereby resulting in a less atherogenic EC phenotype. Current literature indicates that SS is a signal for expression of antiatherogenic genes in cultured ECs, in ECs of isolated arteries, and in ECs of arteries in intact animals. Furthermore, SS levels in the arteries of humans during Ex are in the range that produces beneficial changes. In contrast, complex flow profiles within recirculation zones and/or oscillatory flow patterns can cause proatherogenic gene expression in ECs. In vivo evidence indicates that Ex decreases oscillatory flow/SS in some portions of the arterial tree but may increase oscillatory flow in other areas of the arterial tree. Circumferential wall stress can increase expression of some beneficial EC genes as well, but circumferential wall stress also increases production of reactive oxygen species and increases the expression of adhesion factors and other proatherogenic genes. Interactions of arterial pressure and fluid SS play an important role in arterial vascular health and likely contribute to how Ex bouts signal changes in EC gene expression. It is also clear that other local and circulating factors interact with these hemodynamic signals during Ex to produce the healthy arterial EC phenotype. We conclude that available evidence suggests that exercise signals formation of beneficial endothelial cell phenotype at least in part through changes in SS and wall stretch in the arteries.

Indexed as

ExerciseHemorheologyAdaptation, PhysiologicalAnimalsArteriesAtherosclerosisBlood PressureElasticityEndothelial CellsHumansPhenotypePulsatile FlowSignal TransductionStress, Mechanical

Identifiers

PMID18063803
PMCPMC3289055
OpenAlexW2155065403

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.