Evidence map›Paper›PMID 26458976›Full record

ReviewBiochimie2016

Endothelial cells and cathepsins: Biochemical and biomechanical regulation.

Manu O Platt, W Andrew Shockey

Abstract readReview
In one paragraph

Review in Biochimie, 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
1.1field-weighted citation impact, top 25% 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, 33 citations in OpenAlex.

  1. Article
  2. Review
  3. The mechanism and therapy of aortic aneurysms.Signal transduction and targeted therapy · 2023
    Review
  4. Article
  5. Review
  6. Review
  7. Article
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  9. Article
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  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Engineered nanomaterial-induced lysosomal membrane permeabilization and anti-cathepsin agents.Journal of toxicology and environmental health. Part B, Critical reviews · 2017
    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

2 authors at 1 institution in 1 country.

Manu O PlattWallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University, 950 Atlantic Drive, Suite 3015, Atlanta, GA 30332, USA. Electronic address: manu.platt@bme.gatech.edu.
W Andrew ShockeyWallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University, 950 Atlantic Drive, Suite 3015, Atlanta, GA 30332, USA. Electronic address: ashockey@gatech.edu.
Georgia Institute of Technology · US

Funding

Multiscale, mechanistic, and predictive models of stroke in sickle cell diseaseDP2OD007433 · OD · GEORGIA INSTITUTE OF TECHNOLOGY · PI PLATT, MANU O · 2010 to 2010
$2.3M
NIH HHS DP2 OD007433NIH HHS DP2OD007433
6 · The paper itself

Abstract

Cathepsins are mechanosensitive proteases that are regulated not only by biochemical factors, but are also responsive to biomechanical forces in the cardiovascular system that regulate their expression and activity to participate in cardiovascular tissue remodeling. Their elastinolytic and collagenolytic activity have been implicated in atherosclerosis, abdominal aortic aneurysms, and in heart valve disease, all of which are lined by endothelial cells that are the mechanosensitive monolayer of cells that sense and respond to fluid shear stress as the blood flows across the surfaces of the arteries and valve leaflets. Inflammatory cytokine signaling is integrated with biomechanical signaling pathways by the endothelial cells to transcribe, translate, and activate either the cysteine cathepsins to remodel the tissue or to express their inhibitors to maintain healthy cardiovascular tissue structure. Other cardiovascular diseases should now be included in the study of the cysteine cathepsin activation because of the additional biochemical cues they provide that merges with the already existing hemodynamics driving cardiovascular disease. Sickle cell disease causes a chronic inflammation including elevated TNFα and increased numbers of circulating monocytes that alter the biochemical stimulation while the more viscous red blood cells due to the sickling of hemoglobin alters the hemodynamics and is associated with accelerated elastin remodeling causing pediatric strokes. HIV-mediated cardiovascular disease also occurs earlier in than the broader population and the influence of HIV-proteins and antiretrovirals on endothelial cells must be considered to understand these accelerated mechanisms in order to identify new therapeutic targets for prevention.

Indexed as

Biomechanical PhenomenaAnemia, Sickle CellCardiovascular DiseasesCardiovascular SystemCathepsinsEndothelial CellsHIV InfectionsHumansModels, BiologicalSignal TransductionCathepsinsCardiovascularCathepsinsEndothelial cellsHIVShear stressSickle cell

Identifiers

PMID26458976
PMCPMC4747805
OpenAlexW2178232142

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.