Evidence map›Paper›PMID 33807043›Full record

ReviewInternational journal of molecular sciences2021

Articular Chondrocyte Phenotype Regulation through the Cytoskeleton and the Signaling Processes That Originate from or Converge on the Cytoskeleton: Towards a Novel Understanding of the Intersection between Actin Dynamics and Chondrogenic Function.

Jasmin C Lauer, Mischa Selig, Melanie L Hart, Bodo Kurz, Bernd Rolauffs

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 1 pooled it
10.9field-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

53 citing papers in PubMed, 1 synthesis or guideline pooled it, 92 citations in OpenAlex.

  1. Pooled it
  2. Gold micro-particles for knee osteoarthritis.European journal of pain (London, England) · 2022
    Trial
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  19. Piezo1 promotes intervertebral disc degeneration through the CaMolecular medicine (Cambridge, Mass.) · 2025
    Article
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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

5 authors at 2 institutions in 1 country.

Jasmin C LauerG.E.R.N. Research Center for Tissue Replacement, Regeneration & Neogenesis, Department of Orthopedics and Trauma Surgery, Faculty of Medicine, Medical Center-Albert-Ludwigs-University of Freiburg, 79085 Freiburg im Breisgau, Germany.
Mischa SeligG.E.R.N. Research Center for Tissue Replacement, Regeneration & Neogenesis, Department of Orthopedics and Trauma Surgery, Faculty of Medicine, Medical Center-Albert-Ludwigs-University of Freiburg, 79085 Freiburg im Breisgau, Germany.
Melanie L HartG.E.R.N. Research Center for Tissue Replacement, Regeneration & Neogenesis, Department of Orthopedics and Trauma Surgery, Faculty of Medicine, Medical Center-Albert-Ludwigs-University of Freiburg, 79085 Freiburg im Breisgau, Germany.ORCID 0000-0002-1876-2201
Bodo KurzDepartment of Anatomy, Christian-Albrechts-University, Otto-Hahn-Platz 8, 24118 Kiel, Germany.
Bernd RolauffsG.E.R.N. Research Center for Tissue Replacement, Regeneration & Neogenesis, Department of Orthopedics and Trauma Surgery, Faculty of Medicine, Medical Center-Albert-Ludwigs-University of Freiburg, 79085 Freiburg im Breisgau, Germany.ORCID 0000-0002-3275-8196
University of Freiburg · DEChristian-Albrechts-Universität zu Kiel · DE

Funding

Freiburg University Medical Faculty "Forschungskommission" ROL 1153/17Freiburg University Medical Faculty "Forschungskommission" ROL 1193/18Volkswagen Foundation 92701
6 · The paper itself

Abstract

Numerous studies have assembled a complex picture, in which extracellular stimuli and intracellular signaling pathways modulate the chondrocyte phenotype. Because many diseases are mechanobiology-related, this review asked to what extent phenotype regulators control chondrocyte function through the cytoskeleton and cytoskeleton-regulating signaling processes. Such information would generate leverage for advanced articular cartilage repair. Serial passaging, pro-inflammatory cytokine signaling (TNF-α, IL-1α, IL-1β, IL-6, and IL-8), growth factors (TGF-α), and osteoarthritis not only induce dedifferentiation but also converge on RhoA/ROCK/Rac1/mDia1/mDia2/Cdc42 to promote actin polymerization/crosslinking for stress fiber (SF) formation. SF formation takes center stage in phenotype control, as both SF formation and SOX9 phosphorylation for

Indexed as

ChondrogenesisPhenotypeSignal TransductionActinsAnimalsCell DedifferentiationCell DifferentiationChondrocytesCytoskeletonDisease SusceptibilityHumansProtein BindingProtein IsoformsProtein MultimerizationProtein TransportStress FibersActinsProtein Isoformsactin depolymerizationactin polymerizationchondrocytecollagen aggrecan fragmentscytoskeletonfibrogenic expression profilegrowth factor signalingpro-inflammatory cytokine signalingSOX9stress fiber

Identifiers

PMID33807043
PMCPMC8004672
OpenAlexW3139300088

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.