ArticleJournal of molecular medicine (Berlin, Germany)2016
CLEC5A is critical for dengue virus-induced osteoclast activation and bone homeostasis.
Article in Journal of molecular medicine (Berlin, Germany), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 50 citations in OpenAlex.
- The protective role of MDL-1 in sepsis-induced lung injury: insights from a murine CLP model.Frontiers in immunology · 2026Article
- Pharmacological Evaluation of active compounds in papaya associated with thrombocytopenia inhibition in dengue patients through in silico approaches.Scientific reports · 2025Article
- The C-Type Lectin Receptors.Advances in experimental medicine and biology · 2025Review
- REEP5 mediates the function of CLEC5A to alleviate myocardial infarction by inhibiting endoplasmic reticulum stress-induced apoptosis.BMC cardiovascular disorders · 2024Article
- IL-23 induces CLEC5AJournal of autoimmunity · 2024Article
- Mechanistic insights into bone remodelling dysregulation by human viral pathogens.Nature microbiology · 2024Review
- Identification of potential biomarkers associated with CD4Journal of thoracic disease · 2023Article
- Article
- Interleukin-23 Regulates Inflammatory Osteoclastogenesis via Activation of CLEC5A(+) Osteoclast Precursors.Arthritis & rheumatology (Hoboken, N.J.) · 2023Article
- CLEC5A mediates Zika virus-induced testicular damage.Journal of biomedical science · 2023Article
- Zika virus infects human osteoclasts and blocks differentiation and bone resorption.Emerging microbes & infections · 2022Article
- CLEC5A is critical in Pseudomonas aeruginosa-induced NET formation and acute lung injury.JCI insight · 2022Article
- CLEC5A and TLR2 are critical in SARS-CoV-2-induced NET formation and lung inflammation.Journal of biomedical science · 2022Article
- Medicinal chemistry of the myeloid C-type lectin receptors Mincle, Langerin, and DC-SIGN.RSC medicinal chemistry · 2021Review
- Genetic loss-of-function of activating transcription factor 3 but not C-type lectin member 5A prevents diabetic peripheral neuropathy.Laboratory investigation; a journal of technical methods and pathology · 2021Article
- C-type lectins and extracellular vesicles in virus-induced NETosis.Journal of biomedical science · 2021Review
- Review
- Exploration and Validation of a Novel Inflammatory Response-Associated Gene Signature to Predict Osteosarcoma Prognosis and Immune Infiltration.Journal of inflammation research · 2021Article
- CLEC5A: A Promiscuous Pattern Recognition Receptor to Microbes and Beyond.Advances in experimental medicine and biology · 2020Review
- Extracellular vesicles from CLEC2-activated platelets enhance dengue virus-induced lethality via CLEC5A/TLR2.Nature communications · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 8 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
unlabelledOsteoclasts are bone tissue macrophages critical to maintain bone homeostasis. However, whether osteoclasts are susceptible to flaviviral infections and involved in dengue virus (DV)-induced disease pathogenesis is still unknown. In this study, we found that osteoclasts were preferentially susceptible to DV infection and produced similar amounts of cytokines and infectious virions as macrophages. Interestingly, DV-induced cytokine secretion and nuclear translocation of the transcription factor NFATc1 in osteoclast via the Syk-coupled myeloid C-type lectin member 5A (CLEC5A). Moreover, DV caused transient inflammatory reaction in bone tissue and upregulated osteolytic activity to release C-telopeptide of type I collagen (CTX-1) from bone tissue. Furthermore, DV-induced osteolytic activity was attenuated in CLEC5A-deficient mice, and administration of antagonistic anti-CLEC5A mAb inhibited DV-activated osteolytic activity and reduced CTX-1 serum level in vivo. This observation suggests that osteoclasts serve as a novel target for DV, and transient upregulation of osteolytic activity may contribute to the clinical symptoms in dengue patients. KEY MESSAGES: Cultured osteoclasts were susceptible to DV infection. Osteoclasts produced similar amounts of cytokines and infectious virions as macrophages. DV induced nuclear translocation of NFATc1 in osteoclast via CLEC5A. DV caused transient inflammatory reaction in bone tissue and upregulated osteolytic activity. Antagonistic anti-CLEC5A mAb inhibited DV-activated osteolytic activity in vivo.
Indexed as
Identifiers
What OpenQuestion holds
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.