ArticlePhysiological research2021
Phenotype and function of macrophage polarization in monocrotaline-induced pulmonary arterial hypertension rat model.
Article in Physiological research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed.
- Targeted Delivery of GLUT1 Inhibitor via Macrophage Nanovesicles for Pulmonary Arterial Hypertension Therapy.Journal of extracellular vesicles · 2026Article
- Sphinganine inhibits macrophage polarization and protects against sepsis-induced intestinal injury.World journal of gastroenterology · 2025Article
- In vitro models to mimic tumor endothelial cell-mediated immune cell reprogramming in lung adenocarcinoma.Journal of experimental & clinical cancer research : CR · 2025Article
- Macrophage plasticity and glucose metabolism: the role of immunometabolism in pulmonary arterial hypertension.Clinical science (London, England : 1979) · 2025Review
- The Impact of Proinflammatory M1 Macrophages on the Proliferation and Expression of Cyclin E2, Mitogen-Activated Protein Kinases 4 and 7 in Hepatocytes Isolated from a Diethylnitrosamine-Induced Hepatocellular Carcinoma Rat Model.Molecules (Basel, Switzerland) · 2025Article
- Opposing roles for myeloid and smooth muscle cell STING in pulmonary hypertension.JCI insight · 2025Article
- Changes in Macrophages in Pulmonary Hypertension: A Focus on High-altitude Pulmonary Hypertension.Anatolian journal of cardiology · 2025Review
- Macrophage-driven immunopathology in pulmonary arterial hypertension: from mechanisms to targeted therapies.Frontiers in immunology · 2025Review
- EPA-lactone derivative, 5,6-diHETE lactone, improves pulmonary arterial hypertension in a monocrotaline-induced model.Frontiers in pharmacology · 2025Article
- Mechanisms of lung endothelial cell injury and survival in pulmonary arterial hypertension.American journal of physiology. Lung cellular and molecular physiology · 2024Review
- Emerging connectivity of programmed cell death pathways and pulmonary vascular remodelling during pulmonary hypertension.Journal of cellular and molecular medicine · 2024Review
- Novel insights and new therapeutic potentials for macrophages in pulmonary hypertension.Respiratory research · 2024Review
- PARPs and ADP-Ribosylation in Chronic Inflammation: A Focus on Macrophages.Pathogens (Basel, Switzerland) · 2023Review
- Molecular regulation and therapeutic implications of cell death in pulmonary hypertension.Cell death discovery · 2023Review
- Article
- Impact of l-citrulline on nitric oxide signaling and arginase activity in hypoxic human pulmonary artery endothelial cells.Pulmonary circulation · 2023Article
- Mitochondrial Dysfunction in Pulmonary Hypertension.Antioxidants (Basel, Switzerland) · 2023Review
- Microenvironmental regulation of T-cells in pulmonary hypertension.Frontiers in immunology · 2023Article
- Inflammation and immunity in the pathogenesis of hypoxic pulmonary hypertension.Frontiers in immunology · 2023Review
- Biomarkers in Pulmonary Arterial Hypertension.Diagnostics (Basel, Switzerland) · 2022Review
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pulmonary arterial hypertension (PAH) isa fatal disease characterized by vascular remodeling and chronic inflammation. Macrophages are the key orchestrators of inflammatory and repair responses, and have been demonstrated to be vital in the pathogenesis of PAH. However, specific phenotype of macrophage polarization (M1 & M2 macrophage) in the development of PAH and the underlying mechanisms how they work are still largely unclear. A rat model of monocrotaline (MCT) induced PAH was used. Hemodynamic analysis and histopathological experiments were conducted at day 3, 7, 14, 21 and 28, respectively. In PAH rat lung tissue, confocal microscopic images showed that CD68+NOS2+ M1-like macrophages were remarkably infiltrated on early stage, but dramatically decreased in mid-late stage. Meanwhile, CD68+CD206+ M2-like macrophages in lung tissue accumulated gradually since day 7 to day 28, and the relative ratio of M2/M1 macrophage increased over time. Results detected by western blot and immunohistochemistry were consistent. Further vitro functional studies revealed the possible mechanism involved in this pathophysiological process. By using Transwell co-culture system, it was found that M1 macrophages inducedendothelial cellapoptosis, while M2 macrophages significantly promoted proliferation of both endothelial cell and smooth muscle cell.These data preliminarily demonstrated a temporal dynamic change of macrophage M1/M2 polarization status in the development of experimental PAH. M1 macrophages participated in the initial stage of inflammation by accelerating apoptosis of endothelial cell, while M2 macrophages predominated in the reparative stage of inflammation and the followed stage of aberrant tissue remodeling.
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