ArticleTranslational research : the journal of laboratory and clinical medicine2016
Allergic lung inflammation promotes atherosclerosis in apolipoprotein E-deficient mice.
Article in Translational research : the journal of laboratory and clinical medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed, 19 citations in OpenAlex.
- Associations of the Charlson comorbidity index with asthma and mortality (NHANES 2007-2018): a cross-sectional study.Journal of health, population, and nutrition · 2025Observational
- Apolipoprotein E promoted the proliferation and function of group 2 innate lymphoid cells through low density lipoprotein receptor in allergic rhinitis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
- Differential roles of eosinophils in cardiovascular disease.Nature reviews. Cardiology · 2025Review
- Cellular and Molecular Mechanisms of Mast Cells in Atherosclerotic Plaque Progression and Destabilization.Clinical reviews in allergy & immunology · 2024Review
- Allergic asthma is a risk factor for human cardiovascular diseases.Nature cardiovascular research · 2022Review
- Observational
- Cytokines at the Interplay Between Asthma and Atherosclerosis?Frontiers in pharmacology · 2020Review
Corrections and comments
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Authors and funding
14 authors at 7 institutions in 2 countries.
Funding
Abstract
Inflammation drives asthma and atherosclerosis. Clinical studies suggest that asthmatic patients have a high risk of atherosclerosis. Yet this hypothesis remains uncertain, given that Th2 imbalance causes asthma whereas Th1 immunity promotes atherosclerosis. In this study, chronic allergic lung inflammation (ALI) was induced in mice by ovalbumin sensitization and challenge. Acute ALI was induced in mice by ovalbumin and aluminum sensitization and ovalbumin challenge. Atherosclerosis was produced in apolipoprotein E-deficient (Apoe(-/-)) mice with a Western diet. When chronic ALI and atherosclerosis were produced simultaneously, ALI increased atherosclerotic lesion size, lesion inflammatory cell content, elastin fragmentation, smooth muscle cell (SMC) loss, lesion cell proliferation, and apoptosis. Production of acute ALI before atherogenesis did not affect lesion size, but increased atherosclerotic lesion CD4(+) T cells, lesion SMC loss, angiogenesis, and apoptosis. Production of acute ALI after atherogenesis also did not change atherosclerotic lesion area, but increased lesion elastin fragmentation, cell proliferation, and apoptosis. In mice with chronic ALI and diet-induced atherosclerosis, daily inhalation of a mast cell inhibitor or corticosteroid significantly reduced atherosclerotic lesion T-cell and mast cell contents, SMC loss, angiogenesis, and cell proliferation and apoptosis, although these drugs did not affect lesion area, compared with those that received vehicle treatment. In conclusion, both chronic and acute ALI promote atherogenesis or aortic lesion pathology, regardless whether ALI occurred before, after, or at the same time as atherogenesis. Antiasthmatic medication can efficiently mitigate atherosclerotic lesion pathology.
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Registered trials
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