Evidence map›Paper›PMID 26686737›Full record

ReviewArchives of biochemistry and biophysics2016

The role of endothelial mechanosensitive genes in atherosclerosis and omics approaches.

Rachel D Simmons, Sandeep Kumar, Hanjoong Jo

Abstract readReview
In one paragraph

Review in Archives of biochemistry and biophysics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

35 citing papers in PubMed, 71 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Mechanosensory entities and functionality of endothelial cells.Frontiers in cell and developmental biology · 2024
    Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Modulation of the mitochondrial CaPhysiological reports · 2023
    Article
  13. Article
  14. The mitochondrial CaScientific reports · 2022
    Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Nuclear Mechanosensation and Mechanotransduction in Vascular Cells.Frontiers in cell and developmental biology · 2022
    Review
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 2 institutions in 1 country.

Rachel D SimmonsWallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University, Atlanta, GA, USA.
Sandeep KumarWallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University, Atlanta, GA, USA.
Hanjoong JoWallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University, Atlanta, GA, USA; Division of Cardiology, Emory University, Atlanta, GA, USA. Electronic address: hanjoong.jo@bme.gatech.edu.
Georgia Institute of Technology · USThe Wallace H. Coulter Department of Biomedical Engineering · US

Funding

T cell triggering events and hypertensionP01HL095070 · NHLBI · EMORY UNIVERSITY · PI JO, HANJOONG · 2009 to 2019
$20.5M
Shear stress, endothelial miRNAs, and AV calcificationR01HL119798 · NHLBI · EMORY UNIVERSITY · PI JO, HANJOONG, YOGANATHAN, AJIT P · 2013 to 2022
$4.7M
Metabolomics of subclinical and clinical cardiovascular diseaseP20HL113451 · NHLBI · EMORY UNIVERSITY · PI JONES, DEAN PAUL · 2012 to 2016
$4.3M
Image-based analysis of miRNA deliveryR01HL124879 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI FERRARA, KATHERINE W, JO, HANJOONG · 2014 to 2017
$3.1M
NHLBI NIH HHS HL095070NHLBI NIH HHS HL113451NHLBI NIH HHS HL119798NHLBI NIH HHS HL124879NHLBI NIH HHS P01 HL095070NHLBI NIH HHS P20 HL113451NHLBI NIH HHS R01 HL119798NHLBI NIH HHS R01 HL124879
6 · The paper itself

Abstract

Atherosclerosis is the leading cause of morbidity and mortality in the U.S., and is a multifactorial disease that preferentially occurs in regions of the arterial tree exposed to disturbed blood flow. The detailed mechanisms by which d-flow induces atherosclerosis involve changes in the expression of genes, epigenetic patterns, and metabolites of multiple vascular cells, especially endothelial cells. This review presents an overview of endothelial mechanobiology and its relation to the pathogenesis of atherosclerosis with special reference to the anatomy of the artery and the underlying fluid mechanics, followed by a discussion of a variety of experimental models to study the role of fluid mechanics and atherosclerosis. Various in vitro and in vivo models to study the role of flow in endothelial biology and pathobiology are discussed in this review. Furthermore, strategies used for the global profiling of the genome, transcriptome, miR-nome, DNA methylome, and metabolome, as they are important to define the biological and pathophysiological mechanisms of atherosclerosis. These "omics" approaches, especially those which derive data based on a single animal model, provide unprecedented opportunities to not only better understand the pathophysiology of atherosclerosis development in a holistic and integrative manner, but also to identify novel molecular and diagnostic targets.

Indexed as

Blood Flow VelocityMechanotransduction, CellularAnimalsAtherosclerosisBlood PressureEndothelium, VascularHumansProteomeProteomicsProteomeAtherosclerosisBlood flowEndothelial cellsEpigenomicsGenomicsMechanosensitiveMetabolomicsmiRNomicsShear stress

Identifiers

PMID26686737
PMCPMC4747676
OpenAlexW2193732010

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.