ArticleScientific reports2016
ATX-LPA1 axis contributes to proliferation of chondrocytes by regulating fibronectin assembly leading to proper cartilage formation.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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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.
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.
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Who cites it
13 citing papers in PubMed, 34 citations in OpenAlex.
- Phospholipids and Sphingolipids in Osteoarthritis.Biomolecules · 2025Review
- Mutations in fibronectin dysregulate chondrogenesis in skeletal dysplasia.Cellular and molecular life sciences : CMLS · 2024Article
- Autotaxin/Lysophosphatidic Acid Axis: From Bone Biology to Bone Disorders.International journal of molecular sciences · 2022Review
- Lysophospholipid Mediators in Health and Disease.Annual review of pathology · 2022Review
- An ATX-LPAiScience · 2021Article
- Zebrafish Models for Human Skeletal Disorders.Frontiers in genetics · 2021Review
- Loss of FOXF1 expression promotes human lung-resident mesenchymal stromal cell migration via ATX/LPA/LPA1 signaling axis.Scientific reports · 2020Article
- Review
- Osteoclast-Derived Autotaxin, a Distinguishing Factor for Inflammatory Bone Loss.Arthritis & rheumatology (Hoboken, N.J.) · 2019Article
- SOX9 is dispensable for the initiation of epigenetic remodeling and the activation of marker genes at the onset of chondrogenesis.Development (Cambridge, England) · 2018Article
- Review
- Autotaxin-lysophosphatidic acid-LPAThe EMBO journal · 2017Article
- Fibronectin 1 promotes migration and invasion of papillary thyroid cancer and predicts papillary thyroid cancer lymph node metastasis.OncoTargets and therapy · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 7 institutions in 3 countries.
Funding
Abstract
The lipid mediator lysophosphatidic acid (LPA) signals via six distinct G protein-coupled receptors to mediate both unique and overlapping biological effects, including cell migration, proliferation and survival. LPA is produced extracellularly by autotaxin (ATX), a secreted lysophospholipase D, from lysophosphatidylcholine. ATX-LPA receptor signaling is essential for normal development and implicated in various (patho)physiological processes, but underlying mechanisms remain incompletely understood. Through gene targeting approaches in zebrafish and mice, we show here that loss of ATX-LPA1 signaling leads to disorganization of chondrocytes, causing severe defects in cartilage formation. Mechanistically, ATX-LPA1 signaling acts by promoting S-phase entry and cell proliferation of chondrocytes both in vitro and in vivo, at least in part through β1-integrin translocation leading to fibronectin assembly and further extracellular matrix deposition; this in turn promotes chondrocyte-matrix adhesion and cell proliferation. Thus, the ATX-LPA1 axis is a key regulator of cartilage formation.
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Registered trials
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.