ArticleJCI insight2018
The metalloproteinase-proteoglycans ADAMTS7 and ADAMTS12 provide an innate, tendon-specific protective mechanism against heterotopic ossification.
Article in JCI insight, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 46 citations in OpenAlex.
- Review
- Stage-Specific Collagen V Knockdown Reveals Temporal Control of Fibrillogenesis, Remodeling, and Mechanics in Tendon Healing.International journal of molecular sciences · 2026Article
- Decorin inhibits the migration and invasion of the LPS + high glucose-induced primary trophoblast cell through ADAMTS12.In vitro cellular & developmental biology. Animal · 2026Article
- An Overview of ADAMTS Proteases.Methods in molecular biology (Clifton, N.J.) · 2026Review
- Extracellular matrix in vascular homeostasis and disease.Nature reviews. Cardiology · 2025Review
- ADAMTS7, a target in atherosclerosis, cooperates with its homolog ADAMTS12 to protect against myxomatous valve degeneration.Journal of molecular and cellular cardiology plus · 2025Article
- ADAMTS12 serves as a novel prognostic biomarker and promotes proliferation and invasion in gastric cancer.Discover oncology · 2024Article
- Combined genetic-pharmacologic inactivation of tightly linked ADAMTS proteases in temporally specific windows uncovers distinct roles for versican proteolysis and glypican-6 in cardiac development.Matrix biology : journal of the International Society for Matrix Biology · 2024Article
- Article
- BAY-9835: Discovery of the First Orally Bioavailable ADAMTS7 Inhibitor.Journal of medicinal chemistry · 2024Article
- Investigation into the association ofOpen life sciences · 2024Article
- Article
- Proteolysis: a key post-translational modification regulating proteoglycans.American journal of physiology. Cell physiology · 2022Review
- Article
- Article
- Article
- TAILS Identifies Candidate Substrates and Biomarkers of ADAMTS7, a Therapeutic Protease Target in Coronary Artery Disease.Molecular & cellular proteomics : MCP · 2022Article
- Article
- Hedgehog signaling underlying tendon and enthesis development and pathology.Matrix biology : journal of the International Society for Matrix Biology · 2022Review
- Coronary Disease Association With ADAMTS7 Is Due to Protease Activity.Circulation research · 2021Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Heterotopic ossification (HO) is a significant clinical problem with incompletely resolved mechanisms. Here, the secreted metalloproteinases ADAMTS7 and ADAMTS12 are shown to comprise a unique proteoglycan class that protects against a tendency toward HO in mouse hindlimb tendons, menisci, and ligaments. Adamts7 and Adamts12 mRNAs were sparsely expressed in murine forelimbs but strongly coexpressed in hindlimb tendons, skeletal muscle, ligaments, and meniscal fibrocartilage. Adamts7-/- Adamts12-/- mice, but not corresponding single-gene mutants, which demonstrated compensatory upregulation of the intact homolog mRNA, developed progressive HO in these tissues after 4 months of age. Adamts7-/- Adamts12-/- tendons had abnormal collagen fibrils, accompanied by reduced levels of the small leucine-rich proteoglycans (SLRPs) biglycan, fibromodulin, and decorin, which regulate collagen fibrillogenesis. Bgn-/0 Fmod-/- mice are known to have a strikingly similar hindlimb HO to that of Adamts7-/- Adamts12-/- mice, implicating fibromodulin and biglycan reduction as a likely mechanism underlying HO in Adamts7-/- Adamts12-/- mice. Interestingly, degenerated human biceps tendons had reduced ADAMTS7 mRNA compared with healthy biceps tendons, which expressed both ADAMTS7 and ADAMTS12. These results suggest that ADAMTS7 and ADAMTS12 drive an innate pathway protective against hindlimb HO in mice and may be essential for human tendon health.
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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.