Evidence map›Paper›PMID 33322030›Full record

ReviewInternational journal of molecular sciences2020

Involvement of the FAK Network in Pathologies Related to Altered Mechanotransduction.

Enrica Urciuoli, Barbara Peruzzi

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

24 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Curated set of tool compounds to probe PYK2 and FAK signaling in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  6. Review
  7. Review
  8. CRB2 depletion induces YAP signaling and disrupts mechanosensing in podocytes.American journal of physiology. Renal physiology · 2025
    Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Review
  14. Review
  15. Review
  16. Article
  17. Review
  18. Review
  19. Hydrogels for Salivary Gland Tissue Engineering.Gels (Basel, Switzerland) · 2022
    Review
  20. 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.

Enrica UrciuoliMultifactorial Disease and Complex Phenotype Research Area, Bambino Gesù Children's Hospital, IRCCS, 00165 Rome, Italy.ORCID 0000-0002-9746-1668
Barbara PeruzziMultifactorial Disease and Complex Phenotype Research Area, Bambino Gesù Children's Hospital, IRCCS, 00165 Rome, Italy.ORCID 0000-0003-1820-5816
Bambino Gesù Children's Hospital · IT

Funding

Italian Ministry of Health Ricerca Corrente 2020
6 · The paper itself

Abstract

Mechanotransduction is a physiological process in which external mechanical stimulations are perceived, interpreted, and translated by cells into biochemical signals. Mechanical stimulations exerted by extracellular matrix stiffness and cell-cell contacts are continuously applied to living cells, thus representing a key pivotal trigger for cell homeostasis, survival, and function, as well as an essential factor for proper organ development and metabolism. Indeed, a deregulation of the mechanotransduction process consequent to gene mutations or altered functions of proteins involved in perceiving cellular and extracellular mechanics can lead to a broad range of diseases, from muscular dystrophies and cardiomyopathies to cancer development and metastatization. Here, we recapitulate the involvement of focal adhesion kinase (FAK) in the cellular conditions deriving from altered mechanotransduction processes.

Indexed as

Mechanotransduction, CellularAnimalsBone DiseasesCardiomyopathiesExtracellular MatrixFocal Adhesion Protein-Tyrosine KinasesHumansFocal Adhesion Protein-Tyrosine Kinasesextracellular matrixFocal Adhesion Kinase (FAK)focal adhesionsmechanotransductiontissue matrix stiffness

Identifiers

PMID33322030
PMCPMC7764271
OpenAlexW3110657965

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.