ReviewAnatomical record (Hoboken, N.J. : 2007)2020
Genetic Disorders of the Extracellular Matrix.
Review in Anatomical record (Hoboken, N.J. : 2007), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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.
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.
Who cites it
55 citing papers in PubMed, 107 citations in OpenAlex.
- SNED1 fibrillar assembly in the extracellular matrix requires fibronectin and collagen I.Journal of cell science · 2026Article
- SNED1 modulates ECM architecture and cell proliferation via its LDV integrin-binding motif.Journal of cell science · 2026Article
- Beyond DNA damage: 3D tumor models and the integrin mechanobiology of radioresistance.Journal of experimental & clinical cancer research : CR · 2026Review
- Rare protein-coding variation and the genetic architecture of height in >1.4 million individuals.medRxiv : the preprint server for health sciences · 2026Article
- TNBC Spatial Transcriptomic Analysis across Clinical States Reveals Subtype-Specific Networks and Immunosuppressive Niches.Cancer research communications · 2026Article
- SNED1 fibrillar assembly in the extracellular matrix requires fibronectin and collagen I.bioRxiv : the preprint server for biology · 2026Article
- SNED1 modulates ECM architecture and cell proliferation via LDV-binding integrins.bioRxiv : the preprint server for biology · 2026Article
- The extracellular matrix genebioRxiv : the preprint server for biology · 2026Article
- Emerging concepts in osteoarthritis and musculoskeletal diseases: Insights from the University of Debrecen Musculoskeletal Symposium 2025.Osteoarthritis and cartilage open · 2026Article
- The Fibrillar Collagens of Bony Fish: Genes, Proteins, and Biomedical Applications.Sub-cellular biochemistry · 2026Review
- Extracellular ERp57 promotes fibronectin fibril formation during matrix assembly of articular cartilage.iScience · 2025Article
- Review
- Whole genome sequencing in adolescent idiopathic scoliosis cohort implicates multiple biological pathways.NPJ genomic medicine · 2025Article
- Cell-cell communication dysregulation in tuberous sclerosis complex cortical tubers and focal cortical dysplasia.Acta neuropathologica communications · 2025Article
- Molecular Consequences ofInternational journal of molecular sciences · 2025Article
- MatriCom, a single-cell RNA-sequencing data mining tool to infer cell-extracellular matrix interactions.Journal of cell science · 2025Article
- Transcriptomic Profiling of Zebrafish Mutant forInternational journal of molecular sciences · 2025Article
- A Fluid Dynamic In Vitro System to Study the Effect of Hyaluronic Acid Administration on Collagen Organization in Human Skin Explants.International journal of molecular sciences · 2025Article
- Plasma exosome proteomics reveals upregulation of CILP-1 in concave side of paraspinal muscle in adolescent idiopathic scoliosis.Clinical proteomics · 2025Article
- Benzo[a]pyrene-Induced Developmental Toxicity inToxics · 2025Article
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
No grant is acknowledged in the PubMed record.
Abstract
Mutations in the genes for extracellular matrix (ECM) components cause a wide range of genetic connective tissues disorders throughout the body. The elucidation of mutations and their correlation with pathology has been instrumental in understanding the roles of many ECM components. The pathological consequences of ECM protein mutations depend on its tissue distribution, tissue function, and on the nature of the mutation. The prevalent paradigm for the molecular pathology has been that there are two global mechanisms. First, mutations that reduce the production of ECM proteins impair matrix integrity largely due to quantitative ECM defects. Second, mutations altering protein structure may reduce protein secretion but also introduce dominant negative effects in ECM formation, structure and/or stability. Recent studies show that endoplasmic reticulum (ER) stress, caused by mutant misfolded ECM proteins, makes a significant contribution to the pathophysiology. This suggests that targeting ER-stress may offer a new therapeutic strategy in a range of ECM disorders caused by protein misfolding mutations. Anat Rec, 2019. © 2019 The Authors. The Anatomical Record published by Wiley Periodicals, Inc. on behalf of American Association of Anatomists.
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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.