Evidence map›Paper›PMID 36849594›Full record

ReviewNature reviews. Molecular cell biology2023

Cell-extracellular matrix mechanotransduction in 3D.

Aashrith Saraswathibhatla, Dhiraj Indana, Ovijit Chaudhuri

Open access · greenAbstract readReview
In one paragraph

Review in Nature reviews. Molecular cell biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 437 papers.

0numbers the graph read from it
0cells of the map it votes in
437citing papers in PubMed
134.3field-weighted citation impact, top 1% 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

437 citing papers in PubMed, 645 citations in OpenAlex.

  1. Review
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  11. Mechanical regulation of cell memory.Nature structural & molecular biology · 2026
    Review
  12. High-Density Type I Collagen Promotes IFN-γAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  13. Article
  14. Review
  15. Understanding and targeting the tumour matrisome.Nature reviews. Clinical oncology · 2026
    Review
  16. Review
  17. Article
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  20. Article

377 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Aashrith Saraswathibhatla *Department of Mechanical Engineering, Stanford University, Stanford, CA, USA.ORCID 0000-0002-0971-8065
Dhiraj Indana *Department of Mechanical Engineering, Stanford University, Stanford, CA, USA.ORCID 0000-0002-8644-5048
Ovijit ChaudhuriDepartment of Mechanical Engineering, Stanford University, Stanford, CA, USA. chaudhuri@stanford.edu.ORCID 0000-0002-9287-3401
Stanford University · US

Funding

Role of extracellular matrix malleability in mediating breast cancer cell invasion and migrationR37CA214136 · NCI · STANFORD UNIVERSITY · PI CHAUDHURI, OVIJIT · 2018 to 2024
$2.5M
NCI NIH HHS R37 CA214136
6 · The paper itself

Abstract

Mechanical properties of extracellular matrices (ECMs) regulate essential cell behaviours, including differentiation, migration and proliferation, through mechanotransduction. Studies of cell-ECM mechanotransduction have largely focused on cells cultured in 2D, on top of elastic substrates with a range of stiffnesses. However, cells often interact with ECMs in vivo in a 3D context, and cell-ECM interactions and mechanisms of mechanotransduction in 3D can differ from those in 2D. The ECM exhibits various structural features as well as complex mechanical properties. In 3D, mechanical confinement by the surrounding ECM restricts changes in cell volume and cell shape but allows cells to generate force on the matrix by extending protrusions and regulating cell volume as well as through actomyosin-based contractility. Furthermore, cell-matrix interactions are dynamic owing to matrix remodelling. Accordingly, ECM stiffness, viscoelasticity and degradability often play a critical role in regulating cell behaviours in 3D. Mechanisms of 3D mechanotransduction include traditional integrin-mediated pathways that sense mechanical properties and more recently described mechanosensitive ion channel-mediated pathways that sense 3D confinement, with both converging on the nucleus for downstream control of transcription and phenotype. Mechanotransduction is involved in tissues from development to cancer and is being increasingly harnessed towards mechanotherapy. Here we discuss recent progress in our understanding of cell-ECM mechanotransduction in 3D.

Indexed as

Extracellular MatrixMechanotransduction, CellularActin CytoskeletonCell DifferentiationIntegrinsIntegrins

Identifiers

PMID36849594
PMCPMC10656994
OpenAlexW4322493855

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.