ArticleThe American journal of pathology2009
Inhibition of prostaglandin D synthase suppresses muscular necrosis.
Article in The American journal of pathology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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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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Who cites it
27 citing papers in PubMed, 53 citations in OpenAlex.
- Early phase 2 trial of TAS-205 in patients with Duchenne muscular dystrophy.Annals of clinical and translational neurology · 2020Trial
- Dietary omega-6 arachidonic acid and omega-3 docosahexaenoic acid supplementation differentially impact skeletal muscle inflammaging in mice.bioRxiv : the preprint server for biology · 2026Article
- Optimizing linker rigidity to improve intracellular behavior of PROTACs targeting hematopoietic prostaglandin D synthase.RSC medicinal chemistry · 2025Article
- Pharmacology and macrophage modulation of HPGDS inhibitor PK007 demonstrate reduced disease severity in DMD-affected muscles of the mdx mouse model.Skeletal muscle · 2025Article
- Phase 1 Mass Balance Study of Pizuglanstat: An Investigational Hematopoietic Prostaglandin D Synthase Inhibitor.Clinical pharmacology in drug development · 2025Article
- Urinary prostaglandin DScientific reports · 2025Article
- Hematopoietic Prostaglandin D Synthase Is Increased in Mast Cells and Pericytes in Autopsy Myocardial Specimens from Patients with Duchenne Muscular Dystrophy.International journal of molecular sciences · 2024Article
- Targeted genetic therapies for inherited disorders that affect both cardiac and skeletal muscle.Experimental physiology · 2024Review
- Establishment of a Triple Quadrupole HPLC-MS Quantitation Method for Dystrophin Protein in Mouse and Human Skeletal Muscle.International journal of molecular sciences · 2023Article
- Targeting the DP2 receptor alleviates muscle atrophy and diet-induced obesity in mice through oxidative myofiber transition.Journal of cachexia, sarcopenia and muscle · 2023Article
- Structure-activity relationship study of PROTACs against hematopoietic prostaglandin DRSC medicinal chemistry · 2022Article
- Hematopoietic Prostaglandin D Synthase Inhibitor PK007 Decreases Muscle Necrosis in DMDLife (Basel, Switzerland) · 2021Article
- Review
- Prostaglandin DPhysiological reports · 2019Article
- Delay in hepatocyte proliferation and prostaglandin D2 synthase expression for cholestasis due to endotoxin during partial hepatectomy in rats.Molecular medicine reports · 2019Article
- Lipocalin-Like Prostaglandin D Synthase but Not Hemopoietic Prostaglandin D Synthase Deletion Causes Hypertension and Accelerates Thrombogenesis in Mice.The Journal of pharmacology and experimental therapeutics · 2018Article
- A phase I study of TAS-205 in patients with Duchenne muscular dystrophy.Annals of clinical and translational neurology · 2018Article
- Macrophages programmed by apoptotic cells inhibit epithelial-mesenchymal transition in lung alveolar epithelial cells via PGE2, PGD2, and HGF.Scientific reports · 2016Article
- Recent advances in innovative therapeutic approaches for Duchenne muscular dystrophy: from discovery to clinical trials.American journal of translational research · 2016Review
- The skeletal muscle arachidonic acid cascade in health and inflammatory disease.Nature reviews. Rheumatology · 2014Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Duchenne muscular dystrophy is a fatal muscle wasting disease that is characterized by a deficiency in the protein dystrophin. Previously, we reported that the expression of hematopoietic prostaglandin D synthase (HPGDS) appeared in necrotic muscle fibers from patients with either Duchenne muscular dystrophy or polymyositis. HPGDS is responsible for the production of the inflammatory mediator, prostaglandin D(2). In this paper, we validated the hypothesis that HPGDS has a role in the etiology of muscular necrosis. We investigated the expression of HPGDS/ prostaglandin D(2) signaling using two different mouse models of muscle necrosis, that is, bupivacaine-induced muscle necrosis and the mdx mouse, which has a genetic muscular dystrophy. We treated each mouse model with the HPGDS-specific inhibitor, HQL-79, and measured both necrotic muscle volume and selected cytokine mRNA levels. We confirmed that HPGDS expression was induced in necrotic muscle fibers in both bupivacaine-injected muscle and mdx mice. After administration of HQL-79, necrotic muscle volume was significantly decreased in both mouse models. Additionally, mRNA levels of both CD11b and transforming growth factor beta1 were significantly lower in HQL-79-treated mdx mice than in vehicle-treated animals. We also demonstrated that HQL-79 suppressed prostaglandin D(2) production and improved muscle strength in the mdx mouse. Our results show that HPGDS augments inflammation, which is followed by muscle injury. Furthermore, the inhibition of HPGDS ameliorates muscle necrosis even in cases of genetic muscular dystrophy.
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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.