ArticleeLife2014
Thrombospondin-4 controls matrix assembly during development and repair of myotendinous junctions.
Article in eLife, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 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.
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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
74 citing papers in PubMed, 133 citations in OpenAlex.
- SC-framework: A robust and FAIR semi-interactive environment for single-cell resolution datasets.iScience · 2026Article
- Myotendinous Junction development and repair.Journal of orthopaedic translation · 2026Review
- Gene regulatory programs underlying diversification of facial ligaments and tendons in zebrafish.Development (Cambridge, England) · 2026Article
- Analysis of cranial tenocyte heterogeneity reveals a role for Wnt signaling in tendon attachments.Development (Cambridge, England) · 2026Article
- Extracellular matrix deposition precedes muscle-tendon integration during murine forelimb morphogenesis.Communications biology · 2025Article
- Article
- Integrated transcriptomic analysis reveals evolutionary and developmental characteristics of tendon ossification in teleost.BMC biology · 2024Article
- Thrombospondins: Conserved mediators and modulators of metazoan extracellular matrix.International journal of experimental pathology · 2024Review
- Mechanobiological Strategies to Enhance Ovine (Animals : an open access journal from MDPI · 2024Article
- Notochord segmentation in zebrafish controlled by iterative mechanical signaling.Developmental cell · 2024Article
- The extracellular matrix differentially directs myoblast motility and differentiation in distinct forms of muscular dystrophy: Dystrophic matrices alter myoblast motility.Matrix biology : journal of the International Society for Matrix Biology · 2024Article
- Assessing the functional potential of conditioned media derived from amniotic epithelial stem cells engineered on 3D biomimetic scaffolds: An in vitro model for tendon regeneration.Materials today. Bio · 2024Article
- Thrombospondins modulate cell function and tissue structure in the skeleton.Seminars in cell & developmental biology · 2024Review
- Serious Game with Electromyography Feedback and Physical Therapy in Young Children with Unilateral Spastic Cerebral Palsy and Equinus Gait: A Prospective Open-Label Study.Sensors (Basel, Switzerland) · 2024Article
- The super-healing MRL strain promotes muscle growth in muscular dystrophy through a regenerative extracellular matrix.JCI insight · 2024Article
- Single-cell analysis reveals distinct fibroblast plasticity during tenocyte regeneration in zebrafish.Science advances · 2023Article
- Extracellular matrix contribution to disease progression and dysfunction in myopathy.American journal of physiology. Cell physiology · 2023Review
- Mechanical force regulates Sox9 expression at the developing enthesis.Development (Cambridge, England) · 2023Article
- Directionality of developing skeletal muscles is set by mechanical forces.Nature communications · 2023Article
- Axial segmentation by iterative mechanical signaling.bioRxiv : the preprint server for biology · 2023Article
14 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Tendons are extracellular matrix (ECM)-rich structures that mediate muscle attachments with the skeleton, but surprisingly little is known about molecular mechanisms of attachment. Individual myofibers and tenocytes in Drosophila interact through integrin (Itg) ligands such as Thrombospondin (Tsp), while vertebrate muscles attach to complex ECM fibrils embedded with tenocytes. We show for the first time that a vertebrate thrombospondin, Tsp4b, is essential for muscle attachment and ECM assembly at myotendinous junctions (MTJs). Tsp4b depletion in zebrafish causes muscle detachment upon contraction due to defects in laminin localization and reduced Itg signaling at MTJs. Mutation of its oligomerization domain renders Tsp4b unable to rescue these defects, demonstrating that pentamerization is required for ECM assembly. Furthermore, injected human TSP4 localizes to zebrafish MTJs and rescues muscle detachment and ECM assembly in Tsp4b-deficient embryos. Thus Tsp4 functions as an ECM scaffold at MTJs, with potential therapeutic uses in tendon strengthening and repair.
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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.