ArticleAmerican journal of physiology. Lung cellular and molecular physiology2011
Eosinophils are necessary for pulmonary arterial remodeling in a mouse model of eosinophilic inflammation-induced pulmonary hypertension.
Article in American journal of physiology. Lung cellular and molecular physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 50 citations in OpenAlex.
- Mechanical force-induced tissue remodelling in a clinically relevant microphysiological model of asthmatic human lungs.Nature biomedical engineering · 2026Article
- Eosinophil-epithelial interactions mediate protective intestinal remodeling during food allergy.bioRxiv : the preprint server for biology · 2026Article
- Elevated plasma eosinophil-derived neurotoxin is associated with echocardiographic pulmonary vascular involvement in stable COPD.Frontiers in medicine · 2026Article
- Identification of Diagnostic Biomarkers Causally Associated With Gut Microbiota and Pulmonary Arterial Hypertension.Pulmonary circulation · 2025Article
- Current Blood Eosinophilia Does Not Predict the Presence of Pulmonary Hypertension in Patients with End-Stage Lung Disease.Journal of clinical medicine · 2025Article
- CCL11 (Eotaxin) Promotes the Advancement of Aging-Related Cardiovascular Diseases.Reviews in cardiovascular medicine · 2025Review
- STAT6 deficiency mitigates the severity of pulmonary arterial hypertension caused by chronic intermittent hypoxia by suppressing Th2-inducing cytokines.Respiratory research · 2025Article
- Article
- Novel Hemodynamic, Vascular Lesion, and Cytokine/Chemokine Differences Regarding Sex in a Pulmonary Arterial Hypertension Model.American journal of respiratory cell and molecular biology · 2024Article
- Adipokines in pulmonary hypertension: angels or demons?Heliyon · 2023Review
- A new immune disease: systemic hypertension.Clinical kidney journal · 2023Review
- Eosinophils protect against pulmonary hypertension through 14-HDHA and 17-HDHA.The European respiratory journal · 2023Article
- Construction of a diagnostic signature and immune landscape of pulmonary arterial hypertension.Frontiers in cardiovascular medicine · 2022Article
- Pulmonary hypertension: Linking inflammation and pulmonary arterial stiffening.Frontiers in immunology · 2022Review
- Heterogeneity of Group 2 Innate Lymphoid Cells Defines Their Pleiotropic Roles in Cancer, Obesity, and Cardiovascular Diseases.Frontiers in immunology · 2022Review
- Adiponectin and Asthma: Knowns, Unknowns and Controversies.International journal of molecular sciences · 2021Review
- Innate Immune Cells and Hypertension: Neutrophils and Neutrophil Extracellular Traps (NETs).Comprehensive Physiology · 2021Review
- Pulmonary hypertension in eosinophilicERJ open research · 2021Article
- Inhibition of CRTH2-mediated Th2 activation attenuates pulmonary hypertension in mice.The Journal of experimental medicine · 2018Article
- Myeloid-Derived Suppressor Cells and Pulmonary Hypertension.International journal of molecular sciences · 2018Review
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
There is increasing evidence that inflammation plays a pivotal role in the pathogenesis of some forms of pulmonary hypertension (PH). We recently demonstrated that deficiency of adiponectin (APN) in a mouse model of PH induced by eosinophilic inflammation increases pulmonary arterial remodeling, pulmonary pressures, and the accumulation of eosinophils in the lung. Based on these data, we hypothesized that APN deficiency exacerbates PH indirectly by increasing eosinophil recruitment. Herein, we examined the role of eosinophils in the development of inflammation-induced PH. Elimination of eosinophils in APN-deficient mice by treatment with anti-interleukin-5 antibody attenuated pulmonary arterial muscularization and PH. In addition, we observed that transgenic mice that are devoid of eosinophils also do not develop pulmonary arterial muscularization in eosinophilic inflammation-induced PH. To investigate the mechanism by which APN deficiency increased eosinophil accumulation in response to an allergic inflammatory stimulus, we measured expression levels of the eosinophil-specific chemokines in alveolar macrophages isolated from the lungs of mice with eosinophilic inflammation-induced PH. In these experiments, the levels of CCL11 and CCL24 were higher in macrophages isolated from APN-deficient mice than in macrophages from wild-type mice. Finally, we demonstrate that the extracts of eosinophil granules promoted the proliferation of pulmonary arterial smooth muscle cells in vitro. These data suggest that APN deficiency may exacerbate PH, in part, by increasing eosinophil recruitment into the lung and that eosinophils could play an important role in the pathogenesis of inflammation-induced PH. These results may have implications for the pathogenesis and treatment of PH caused by vascular inflammation.
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