ArticleScientific reports2016
Genetic and pharmacological inhibition of CDK9 drives neutrophil apoptosis to resolve inflammation in zebrafish in vivo.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 62 citations in OpenAlex.
- Real-time characterisation of microbe-induced inflammation using a novel zebrafish larval corneal injury and infection model.Communications biology · 2026Article
- LARP7 protects against ischemic brain injury by modulating NLRP3 deacetylation to suppress neuronal pyroptosis.Journal of neuroinflammation · 2025Article
- Reactive oxygen species counteract zebrafish wound contraction and promote wound healing.Biophysical journal · 2025Article
- Repurposing flavopiridol as an inhaled therapeutic for pulmonary fibrosis.European journal of pharmacology · 2025Article
- Metainflammation alters neutrophil function and migration in vivo in response to tissue injury.Journal of leukocyte biology · 2025Article
- Temporal dichotomy of neutrophil function in acute liver injury and repair.JHEP reports : innovation in hepatology · 2025Article
- Flavopiridol restores granulopoiesis in experimental models of severe congenital neutropenia.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Drug repurposing of cyclin-dependent kinase inhibitors for neutrophilic acute respiratory distress syndrome and psoriasis.Journal of advanced research · 2025Review
- Inhibition of DYRK1B BY C81 impedes inflammatory processes in leukocytes by reducing STAT3 activity.Cellular and molecular life sciences : CMLS · 2025Article
- Neutrophils facilitate the epicardial regenerative response after zebrafish heart injury.Developmental biology · 2024Article
- Beyond host defense and tissue injury: the emerging role of neutrophils in tissue repair.American journal of physiology. Cell physiology · 2024Review
- Article
- Examination of the Impact of Triazole Position within Linkers on Solubility and Lipophilicity of a CDK9 Degrader Series.ACS medicinal chemistry letters · 2023Article
- Application of transgenic zebrafish for investigating inflammatory responses to nanomaterials: Recommendations for new users.F1000Research · 2023Review
- Delayed neutrophil apoptosis may enhance NET formation in ARDS.Respiratory research · 2022Article
- PROTACs: great opportunities for academia and industry (an update from 2020 to 2021).Signal transduction and targeted therapy · 2022Review
- Pannexin 1 drives efficient epithelial repair after tissue injury.Science immunology · 2022Article
- A curious case of cyclin-dependent kinases in neutrophils.Journal of leukocyte biology · 2022Review
- A preclinical platform for assessing antitumor effects and systemic toxicities of cancer drug targets.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Selective Cdk9 inhibition resolves neutrophilic inflammation and enhances cardiac regeneration in larval zebrafish.Development (Cambridge, England) · 2022Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Neutrophilic inflammation is tightly regulated and subsequently resolves to limit tissue damage and promote repair. When the timely resolution of inflammation is dysregulated, tissue damage and disease results. One key control mechanism is neutrophil apoptosis, followed by apoptotic cell clearance by phagocytes such as macrophages. Cyclin-dependent kinase (CDK) inhibitor drugs induce neutrophil apoptosis in vitro and promote resolution of inflammation in rodent models. Here we present the first in vivo evidence, using pharmacological and genetic approaches, that CDK9 is involved in the resolution of neutrophil-dependent inflammation. Using live cell imaging in zebrafish with labelled neutrophils and macrophages, we show that pharmacological inhibition, morpholino-mediated knockdown and CRISPR/cas9-mediated knockout of CDK9 enhances inflammation resolution by reducing neutrophil numbers via induction of apoptosis after tailfin injury. Importantly, knockdown of the negative regulator La-related protein 7 (LaRP7) increased neutrophilic inflammation. Our data show that CDK9 is a possible target for controlling resolution of inflammation.
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Registered trials
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