Evidence map›Paper›PMID 27295628›Full record

ArticleTranslational research : the journal of laboratory and clinical medicine2016

Atheroprotective laminar flow inhibits Hippo pathway effector YAP in endothelial cells.

Suowen Xu, Marina Koroleva, Meimei Yin, Zheng Gen Jin

Open access · bronzeAbstract read
In one paragraph

Article in Translational research : the journal of laboratory and clinical medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
3.0field-weighted citation impact, top 10% 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

53 citing papers in PubMed, 82 citations in OpenAlex.

  1. Review
  2. Mechanobiology of the Hippo-YAP Signaling Network.Cold Spring Harbor perspectives in biology · 2026
    Article
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  4. Article
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  19. CaCellular signalling · 2023
    Review
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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

4 authors at 2 institutions in 1 country.

Suowen XuAab Cardiovascular Research Institute, Department of Medicine, University of Rochester School of Medicine and Dentistry, Rochester, NY.
Marina KorolevaAab Cardiovascular Research Institute, Department of Medicine, University of Rochester School of Medicine and Dentistry, Rochester, NY.
Meimei YinAab Cardiovascular Research Institute, Department of Medicine, University of Rochester School of Medicine and Dentistry, Rochester, NY.
Zheng Gen JinAab Cardiovascular Research Institute, Department of Medicine, University of Rochester School of Medicine and Dentistry, Rochester, NY. Electronic address: Zheng-gen_Jin@urmc.rochester.edu.
University of Rochester · USRochester Institute of Technology · US

Funding

SIRT6 and vascular endothelial homeostasisR01HL130167 · NHLBI · UNIVERSITY OF ROCHESTER · PI JIN, ZHENG-GEN · 2017 to 2025
$4.2M
Molecular regulation of angiogenesisR01HL114570 · NHLBI · UNIVERSITY OF ROCHESTER · PI JIN, ZHENG-GEN · 2012 to 2016
$1.9M
Regulation of angiogenesis by transcription factorsR01HL128363 · NHLBI · UNIVERSITY OF ROCHESTER · PI JIN, ZHENG-GEN · 2016 to 2019
$1.5M
Regulation of laminar flow atheroprotective genes by HDAC5R01HL109502 · NHLBI · UNIVERSITY OF ROCHESTER · PI JIN, ZHENG-GEN · 2012 to 2015
$1.5M
NHLBI NIH HHS R01 HL109502NHLBI NIH HHS R01 HL114570NHLBI NIH HHS R01 HL128363NHLBI NIH HHS R01 HL130167
6 · The paper itself

Abstract

Atherosclerosis is a mechanobiology-related disease that preferentially develops in the aortic arch and arterial branches, which are exposed to disturbed/turbulent blood flow but less in thoracic aorta where the flow pattern is steady laminar flow (LF). Increasing evidence supports that steady LF with high shear stress is protective against atherosclerosis. However, the molecular mechanisms of LF-mediated atheroprotection remain incompletely understood. Hippo/YAP (yes-associated protein) pathway senses and effects mechanical cues and has been reported to be a master regulator of cell proliferation, differentiation, and tissue homeostasis. Here, we show that LF inhibits YAP activity in endothelial cells (ECs). We observed that YAP is highly expressed in mouse EC-enriched tissues (lung and aorta) and in human ECs. Furthermore, we found in apolipoprotein E deficient (ApoE(-/-)) mice and human ECs, LF decreased the level of nuclear YAP protein and YAP target gene expression (connective tissue growth factor and cysteine-rich protein 61) through promoting Hippo kinases LATS1/2-dependent YAP (Serine 127) phosphorylation. Functionally, we revealed that YAP depletion in ECs phenocopying LF responses, reduced the expression of cell cycle gene cyclin A1 (CCNA1) and proinflammatory gene CCL2 (MCP-1). Taken together, we demonstrate that atheroprotective LF inhibits endothelial YAP activation, which may contribute to LF-mediated ECs quiescence and anti-inflammation.

Indexed as

Coronary CirculationSignal TransductionAdaptor Proteins, Signal TransducingAnimalsAorta, ThoracicAtherosclerosisCell Cycle ProteinsCell NucleusChemokine CCL2Connective Tissue Growth FactorCyclin A1Cysteine-Rich Protein 61Endothelial CellsHumansHuman Umbilical Vein Endothelial CellsMaleAdaptor Proteins, Signal TransducingCCN1 protein, humanCCN2 protein, humanCell Cycle ProteinsChemokine CCL2Connective Tissue Growth FactorCyclin A1Cysteine-Rich Protein 61LATS1 protein, humanLATS2 protein, humanPhosphoproteinsProtein Serine-Threonine KinasesTranscription FactorsTumor Suppressor ProteinsYAP1 protein, humanYap1 protein, mouseYAP-Signaling Proteins

Identifiers

PMID27295628
PMCPMC5116386
OpenAlexW2404556794

What OpenQuestion holds

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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.