Evidence map›Paper›PMID 31585890›Full record

ArticleFrontiers in bioscience (Landmark edition)2020

Simvastatin improves lysosome function via enhancing lysosome biogenesis in endothelial cells.

Youzhi Zhang, Yun-Ting Wang, Saisudha Koka, Yang Zhang, Tahir Hussain, Xiang Li

Open access · bronzeAbstract read
In one paragraph

Article in Frontiers in bioscience (Landmark edition), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

17 citing papers in PubMed, 27 citations in OpenAlex.

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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 2 countries.

Youzhi ZhangSchool of Pharmacy, Hubei University of Science and Technology, Xianning, China.
Yun-Ting WangDepartment of Pharmacological & Pharmaceutical Sciences, College of Pharmacy, University of Houston, Houston, TX 77204.
Saisudha KokaDepartment of Pharmacological & Pharmaceutical Sciences, College of Pharmacy, University of Houston, Houston, TX 77204.
Yang ZhangDepartment of Pharmacology and Toxicology, School of Medicine, Virginia Commonwealth University, Richmond, VA, 23298.
Tahir HussainDepartment of Pharmacological & Pharmaceutical Sciences, College of Pharmacy, University of Houston, Houston, TX 77204.
Xiang LiDepartment of Pharmacological & Pharmaceutical Sciences, College of Pharmacy, University of Houston, Houston, TX 77204, 33TUxli61@central.uh.eduU33T.
Hubei University of Science and Technology · CN

Funding

Subendothelial Exosomes in Coronary Microvascular DysfunctionR01HL075316 · NHLBI · VIRGINIA COMMONWEALTH UNIVERSITY · PI LI, PINLAN · 2004 to 2024
$6.7M
Lysosome Trafficking Dysregulation of Arterial Myocytes in AtherogenesisR01HL122937 · NHLBI · VIRGINIA COMMONWEALTH UNIVERSITY · PI LI, PINLAN, ZHANG, YANG · 2014 to 2024
$4.0M
Endothelial Inflammasomes in Coronary Microcirculation -Beyond InflammationR01HL122769 · NHLBI · VIRGINIA COMMONWEALTH UNIVERSITY · PI ZHANG, YANG · 2014 to 2018
$1.9M
NHLBI NIH HHS R01 HL075316NHLBI NIH HHS R01 HL122769NHLBI NIH HHS R01 HL122937
6 · The paper itself

Abstract

Nlrp3 inflammasomes were shown to play a critical role in triggering obesity-associated early onsets of cardiovascular complications such as endothelial barrier dysfunction with endothelial hyperpermeability. Statins prevent endothelial dysfunction and decrease cardiovascular risk in patients with obesity and diabetes. However, it remains unclear whether statin treatment for obesity-induced endothelial barrier dysfunction is in part due to the blockade of Nlrp3 inflammasome signaling axis. The results showed that simvastatin, a clinically and widely used statin, prevented free fatty acid-induced endothelial hyperpermeability and disruption of ZO-1 and VE-cadherin junctions in mouse microvascular endothelial cells (MVECs). This protective effect of simvastatin was largely due to improved lysosome function that attenuated lysosome injury-mediated Nlrp3 inflammasome activation and subsequent release of high mobility group box protein-1 (HMGB1). Mechanistically, simvastatin induces autophagy that promotes removal of damaged lysosomes and also promotes lysosome regeneration that preserves lysosome function. Collectively, simvastatin treatment improves lysosome function via enhancing lysosome biogenesis and its autophagic turnover, which may be an important mechanism to suppress Nlrp3 inflammasome activation and prevents endothelial hyperpermeability in obesity.

Indexed as

AnimalsAntigens, CDAutophagyCadherin 5CadherinsCells, CulturedCell SurvivalEndothelial CellsHMGB1 ProteinHumansHydroxymethylglutaryl-CoA Reductase InhibitorsInflammasomesLysosomesMiceNLR Family, Pyrin Domain-Containing 3 ProteinSimvastatinAntigens, CDCadherin 5CadherinsHMGB1 ProteinHydroxymethylglutaryl-CoA Reductase InhibitorsInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinSimvastatinTjp1 protein, mouseZonula Occludens-1 Protein

Identifiers

PMID31585890
PMCPMC6812495
OpenAlexW2979047639

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.