ArticleThe Journal of investigative dermatology2017
New Mechanisms of ECM Production during Wound Healing: A Role for Parathyroid Hormone 2 Receptor Signaling.
Article in The Journal of investigative dermatology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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
1 citing paper in PubMed, 7 citations in OpenAlex.
- Transcriptome signatures for the identification of bevacizumab responders in ovarian cancer.Genome medicine · 2026Article
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1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Extracellular matrix deposition is required for wound healing. Studies by Sato et al. reveal a role for parathyroid hormone 2 receptor (PTH2R) in extracellular matrix production in wounds. Deficiencies in PTH2R or its ligand tuberoinfundibular peptide of 39 residues (TIP39) delayed repair, and TIP39 treatment accelerated healing. TIP39-PTH2R signaling induced decorin expression, which may explain the beneficial effects of PTH2R signaling on healing. These studies identify a novel role for PTH2R signaling in extracellular matrix production.
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Registered trials
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