ArticleAmerican journal of physiology. Lung cellular and molecular physiology2019
Chemokine signaling axis between endothelial and myeloid cells regulates development of pulmonary hypertension associated with pulmonary fibrosis and hypoxia.
Article in American journal of physiology. Lung cellular and molecular physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 24 citations in OpenAlex.
- Opposing roles for myeloid and smooth muscle cell STING in pulmonary hypertension.JCI insight · 2025Article
- Lung endothelial cell heterogeneity in health and pulmonary vascular disease.American journal of physiology. Lung cellular and molecular physiology · 2025Review
- Investigation into the role of H2-Ab1 in vascular remodeling in pulmonary arterial hypertension via Bioinformatics.BMC pulmonary medicine · 2024Article
- Role of Sensory Nerves in Pulmonary Fibrosis.International journal of molecular sciences · 2024Review
- Non-Interferon-Dependent Role of STING Signaling in Pulmonary Hypertension.Arteriosclerosis, thrombosis, and vascular biology · 2024Article
- The vascular perspective on acute and chronic lung disease.The Journal of clinical investigation · 2023Review
- Role of myeloid-derived suppressor cells in tumor recurrence.Cancer metastasis reviews · 2023Review
- Myeloid-derived suppressor cells and pulmonary hypertension.Frontiers in immunology · 2023Review
- Article
- Pharmacological modulation of myeloid-derived suppressor cells to dampen inflammation.Frontiers in immunology · 2022Review
- The alterations in molecular markers and signaling pathways in chronic thromboembolic pulmonary hypertension, a study with transcriptome sequencing and bioinformatic analysis.Frontiers in cardiovascular medicine · 2022Article
- A wrinkle in time: circadian biology in pulmonary vascular health and disease.American journal of physiology. Lung cellular and molecular physiology · 2022Article
- A New Antitumor Direction: Tumor-Specific Endothelial Cells.Frontiers in oncology · 2021Review
- Interpreting Immunoregulation in Lung Fibrosis: A New Branch of the Immune Model.Frontiers in immunology · 2021Review
- Emergency myelopoiesis contributes to immune cell exhaustion and pulmonary vascular remodelling.British journal of pharmacology · 2021Article
- Oral 15-Hydroxyeicosatetraenoic Acid Induces Pulmonary Hypertension in Mice by Triggering T Cell-Dependent Endothelial Cell Apoptosis.Hypertension (Dallas, Tex. : 1979) · 2020Article
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11 authors at 2 institutions in 1 country.
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Abstract
Pulmonary hypertension complicates the care of many patients with chronic lung diseases (defined as Group 3 pulmonary hypertension), yet the mechanisms that mediate the development of pulmonary vascular disease are not clearly defined. Despite being the most prevalent form of pulmonary hypertension, to date there is no approved treatment for patients with disease. Myeloid-derived suppressor cells (MDSCs) and endothelial cells in the lung express the chemokine receptor CXCR2, implicated in the evolution of both neoplastic and pulmonary vascular remodeling. However, precise cellular contribution to lung disease is unknown. Therefore, we used mice with tissue-specific deletion of CXCR2 to investigate the role of this receptor in Group 3 pulmonary hypertension. Deletion of CXCR2 in myeloid cells attenuated the recruitment of polymorphonuclear MDSCs to the lungs, inhibited vascular remodeling, and protected against pulmonary hypertension. Conversely, loss of CXCR2 in endothelial cells resulted in worsened vascular remodeling, associated with increased MDSC migratory capacity attributable to increased ligand availability, consistent with analyzed patient sample data. Taken together, these data suggest that CXCR2 regulates MDSC activation, informing potential therapeutic application of MDSC-targeted treatments.
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