Evidence map›Paper›PMID 26715135›Full record

ReviewAntioxidants & redox signaling2016

Blood Brothers: Hemodynamics and Cell-Matrix Interactions in Endothelial Function.

Arif Yurdagul, A Wayne Orr

Open access · greenAbstract readReview
In one paragraph

Review in Antioxidants & redox signaling, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
0.8field-weighted citation impact, top 27% 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

22 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Review
  6. Mechanisms of endothelial flow sensing.Nature cardiovascular research · 2023
    Review
  7. Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Integrin affinity modulation critically regulates atherogenic endothelial activation in vitro and in vivo.Matrix biology : journal of the International Society for Matrix Biology · 2021
    Article
  14. Article
  15. Sinner or Saint?: Nck Adaptor Proteins in Vascular Biology.Frontiers in cell and developmental biology · 2021
    Review
  16. Review
  17. Article
  18. Article
  19. The Importance of Mechanical Forces forFrontiers in physiology · 2020
    Review
  20. Cystathionine γ-Lyase Modulates Flow-Dependent Vascular Remodeling.Arteriosclerosis, thrombosis, and vascular biology · 2018
    Article
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

2 authors at 1 institution in 1 country.

Arif Yurdagul1 Department of Cell Biology and Anatomy, Louisiana State University Health Sciences Center-Shreveport , Shreveport, Louisiana.
A Wayne Orr1 Department of Cell Biology and Anatomy, Louisiana State University Health Sciences Center-Shreveport , Shreveport, Louisiana.
Louisiana State University Health Sciences Center Shreveport · US

Funding

Matrix Signaling in Endothelial Cell DysfunctionR01HL098435 · NHLBI · LOUISIANA STATE UNIV HSC SHREVEPORT · PI ORR, ANTHONY WAYNE · 2010 to 2020
$3.2M
NHLBI NIH HHS R01 HL098435
6 · The paper itself

Abstract

significanceAlterations in endothelial function contribute to a variety of vascular diseases. In pathological conditions, the endothelium shows a reduced ability to regulate vasodilation (endothelial dysfunction) and a conversion toward a proinflammatory and leaky phenotype (endothelial activation). At the interface between the vessel wall and blood, the endothelium exists in a complex microenvironment and must translate changes in these environmental signals to alterations in vessel function. Mechanical stimulation and endothelial cell interactions with the vascular matrix, as well as a host of soluble factors, coordinately contribute to this dynamic regulation. RECENT ADVANCES: Blood hemodynamics play an established role in the regulation of endothelial function. However, a growing body of work suggests that subendothelial matrix composition similarly and coordinately regulates endothelial cell phenotype such that blood flow affects matrix remodeling, which affects the endothelial response to flow. CRITICAL ISSUES: Hemodynamics and soluble factors likely affect endothelial matrix remodeling through multiple mechanisms, including transforming growth factor β signaling and alterations in cell-matrix receptors, such as the integrins. Likewise, differential integrin signaling following matrix remodeling appears to regulate several key flow-induced responses, including nitric oxide production, regulation of oxidant stress, and activation of proinflammatory signaling and gene expression. Microvascular remodeling responses, such as angiogenesis and arteriogenesis, may also show coordinated regulation by flow and matrix. FUTURE DIRECTIONS: Identifying the mechanisms regulating the dynamic interplay between hemodynamics and matrix remodeling and their contribution to the pathogenesis of cardiovascular disease remains an important research area with therapeutic implications across a variety of conditions. Antioxid. Redox Signal. 25, 415-434.

Indexed as

HemodynamicsAnimalsCell AdhesionCell CycleEndothelium, VascularExtracellular MatrixExtracellular Matrix ProteinsHumansIntegrinsMechanotransduction, CellularNeovascularization, PhysiologicProtein BindingShear StrengthSignal TransductionStress, MechanicalExtracellular Matrix ProteinsIntegrins

Identifiers

PMID26715135
PMCPMC5011636
OpenAlexW2274060370

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.