ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2015
Deletion of ADORA2B from myeloid cells dampens lung fibrosis and pulmonary hypertension.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 72 citations in OpenAlex.
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- Decoding fibrosis in nonresolvable COVID-19: a role for myeloid-specific HIF1A deletion.American journal of physiology. Cell physiology · 2025Article
- Decoding the complexity: mechanistic insights into comorbidities in idiopathic pulmonary fibrosis.The European respiratory journal · 2025Review
- Does Adenosine Triphosphate via Purinergic Receptor Signalling Fuel Pulmonary Fibrosis?Journal of innate immunity · 2025Review
- Impact of the adenosine receptor A2BR expressed on myeloid cells on immune regulation during pregnancy.European journal of immunology · 2024Article
- Monocytes and macrophages: emerging mechanisms and novel therapeutic targets in pulmonary fibrosis.American journal of physiology. Cell physiology · 2023Review
- Ivy Leaf Dry Extract EA 575International journal of molecular sciences · 2023Article
- Pharmacology and Emerging Therapies for Group 3 Pulmonary Hypertension Due to Chronic Lung Disease.Pharmaceuticals (Basel, Switzerland) · 2023Review
- A2B Adenosine Receptor in Idiopathic Pulmonary Fibrosis: Pursuing Proper Pit Stop to Interfere with Disease Progression.International journal of molecular sciences · 2023Review
- Hyaluronan in the pathogenesis of acute and post-acute COVID-19 infection.Matrix biology : journal of the International Society for Matrix Biology · 2023Review
- Salt-inducible kinase 2 regulates fibrosis during bleomycin-induced lung injury.The Journal of biological chemistry · 2022Article
- CD39 in the development and progression of pulmonary arterial hypertension.Purinergic signalling · 2022Review
- Chitinase 3 like 1 contributes to the development of pulmonary vascular remodeling in pulmonary hypertension.JCI insight · 2022Article
- A novel definition and treatment of hyperinflammation in COVID-19 based on purinergic signalling.Purinergic signalling · 2022Review
- Adenosine and Inflammation: Here, There and Everywhere.International journal of molecular sciences · 2021Review
- Review
- Idiopathic pulmonary fibrosis and pulmonary hypertension: Heracles meets the Hydra.British journal of pharmacology · 2021Review
Corrections and comments
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Authors and funding
16 authors at 4 institutions in 2 countries.
Funding
Abstract
Idiopathic pulmonary fibrosis (IPF) is a lethal, fibroproliferative disease. Pulmonary hypertension (PH) can develop secondary to IPF and increase mortality. Alternatively, activated macrophages (AAMs) contribute to the pathogenesis of both IPF and PH. Here we hypothesized that adenosine signaling through the ADORA2B on AAMs impacts the progression of these disorders and that conditional deletion of ADORA2B on myeloid cells would have a beneficial effect in a model of these diseases. Conditional knockout mice lacking ADORA2B on myeloid cells (Adora2B(f/f)-LysM(Cre)) were exposed to the fibrotic agent bleomycin (BLM; 0.035 U/g body weight, i.p.). At 14, 17, 21, 25, or 33 d after exposure, SpO2, bronchoalveolar lavage fluid (BALF), and histologic analyses were performed. On day 33, lung function and cardiovascular analyses were determined. Markers for AAM and mediators of fibrosis and PH were assessed. Adora2B(f/f)-LysM(Cre) mice presented with attenuated fibrosis, improved lung function, and no evidence of PH compared with control mice exposed to BLM. These findings were accompanied by reduced expression of CD206 and arginase-1, markers for AAMs. A 10-fold reduction in IL-6 and a 5-fold decrease in hyaluronan, both linked to lung fibrosis and PH, were also observed. These data suggest that activation of the ADORA2B on macrophages plays an active role in the pathogenesis of lung fibrosis and PH.
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