Evidence map›Paper›PMID 29932503›Full record

ArticlePhysiological reports2018

Physical activity protects NLRP3 inflammasome-associated coronary vascular dysfunction in obese mice.

Jonghae Lee, Yang Lee, Emily C LaVoy, Michihisa Umetani, Junyoung Hong, Yoonjung Park

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Physiological reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.5field-weighted citation impact, top 16% 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

19 citing papers in PubMed, 26 citations in OpenAlex.

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  15. NLRP3 Inflammasome in Diabetic Cardiomyopathy and Exercise Intervention.International journal of molecular sciences · 2021
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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 2 institutions in 1 country.

Jonghae LeeLaboratory of Integrated Physiology, Department of Health and Human Performance, University of Houston, Houston, Texas.
Yang LeeTexas A&M Health Science College of Medicine, College Station, Texas.
Emily C LaVoyLaboratory of Integrated Physiology, Department of Health and Human Performance, University of Houston, Houston, Texas.
Michihisa UmetaniDepartment of Biology and Biochemistry, University of Houston, Houston, Texas.
Junyoung HongLaboratory of Integrated Physiology, Department of Health and Human Performance, University of Houston, Houston, Texas.
Yoonjung ParkLaboratory of Integrated Physiology, Department of Health and Human Performance, University of Houston, Houston, Texas.
University of Houston · USTexas A&M Health Science Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Activation of the nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome mediates the release of pro-inflammatory cytokine interleukin (IL)-1β and thereby plays a pivotal role in the inflammatory response in vascular pathology. An active lifestyle has beneficial effects on inflammation-associated vascular dysfunction in obesity. However, it remains unclear how physical activity regulates NLRP3 inflammasome-mediated vascular dysfunction in obesity. Therefore, we explored the protective effect of physical activity on NLRP3 inflammasome-associated vascular dysfunction in mouse hearts, and the potential underlying mechanisms. C57BL/6J male mice were randomly divided into four groups: (1) control low-fat diet (LF-SED), (2) LF diet with free access to a voluntary running wheel (LF-RUN), (3) high-fat diet (HF-SED; 45% of calories from fat), and (4) HF-RUN. We examined NLRP3 inflammasome-related signaling pathways, nitric oxide (NO) signaling, and oxidative stress in coronary arterioles to test effects of HFD and physical activity. Voluntary running reduced NLRP3 inflammasome and its downstream effects, caspase-1 and IL-1β in coronary arteriole endothelium of obese mice in immunofluorescence staining. HF-RUN attenuated HFD-dependent endothelial NO synthase (eNOS) reduction and thus increased NO production compared to HF-SED. HFD elevated intracellular superoxide production in coronary arterioles while voluntary running ameliorated oxidative stress. Our findings provide the first evidence that voluntary running attenuates endothelial NLRP3 inflammasome activation in coronary arterioles of HFD feeding mice. Results further suggest that voluntary running improves obesity-induced vascular dysfunction by preserved NO bioavailability via restored expression of eNOS and reduced oxidative stress.

Indexed as

AnimalsArteriolesCoronary Artery DiseaseCoronary VesselsDiet, Fat-RestrictedDiet, High-FatInflammasomesMaleMice, Inbred C57BLMice, ObeseMotor ActivityNitric OxideNLR Family, Pyrin Domain-Containing 3 ProteinObesityOxidative StressSignal TransductionInflammasomesNitric OxideNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseDiet-induced obesityinflammationvascular functionvoluntary running

Identifiers

PMID29932503
PMCPMC6014451
OpenAlexW2808832289

What Socratic holds

Textmetadata
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 Socratic graph.