ArticleJournal of immunology (Baltimore, Md. : 1950)2023
JMJD3 Is Required for Acute Pancreatitis and Pancreatitis-Associated Lung Injury.
Article in Journal of immunology (Baltimore, Md. : 1950), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Targeting the Cyclic GMP-AMP Synthase-Stimulator of Interferon Genes Pathway: An Emerging Therapeutic Strategy for Digestive Diseases.Clinical and translational gastroenterology · 2026Review
- Severe Acute Pancreatitis-Associated Lung Injury: A Comprehensive Quadruple Analysis of Animal Models.Digestive diseases and sciences · 2025Article
- Predictive biomarkers for post-neonatal necrotizing enterocolitis intestinal stenosis: Role of JMJD3, CRP, and PCT.Biomolecules & biomedicine · 2025Article
- Mitochondrial DNA signals driving immune responses: Why, How, Where?Cell communication and signaling : CCS · 2025Review
- cGAS-STING targeting offers therapy choice in lung diseases.Biology direct · 2025Review
- cGAS-STING pathway as a promising target for digestive diseases: insights from natural plant products.Frontiers in nutrition · 2025Review
- Emerging role of Jumonji domain-containing protein D3 in inflammatory diseases.Journal of pharmaceutical analysis · 2024Review
- The role and regulation of SIRT1 in pulmonary fibrosis.Molecular biology reports · 2024Review
Corrections and comments
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Authors and funding
26 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute pancreatitis (AP) can be complicated by inflammatory disorders of remote organs, such as lung injury, in which Jumonji domain-containing protein 3 (JMJD3) plays a vital role in proinflammatory responses. Currently, we found that JMJD3 expression was upregulated in the pancreas and lung in an AP male mouse model, which was also confirmed in AP patients. Further experiments revealed that the upregulation of JMJD3 and proinflammatory effects were possibly exerted by mitochondrial DNA (mtDNA) or oxidized-mtDNA from tissue injury caused by AP. The release of mtDNA and oxidized-mtDNA contributed to the infiltration of inflammatory monocytes in lung injury through the stimulator of IFN genes (STING)/TLR9-NF-κB-JMJD3-TNF-α pathway. The inhibition of JMJD3 or utilization of Jmjd3-cKO mice significantly alleviated pulmonary inflammation induced by AP. Blocking mtDNA oxidation or knocking down the TLR9/STING pathway effectively alleviated inflammation. Therefore, inhibition of JMJD3 or STING/TLR9 pathway blockage might be a potential therapeutic strategy to treat AP and the associated lung injury.
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Registered trials
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