ArticleInternational journal of vascular medicine2012
A Model of Left Ventricular Dysfunction Complicated by CAWS Arteritis in DBA/2 Mice.
Article in International journal of vascular medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- Statin suppresses the development of excessive intimal proliferation in a Kawasaki disease mouse model.Physiological reports · 2024Article
- Red ginseng prevents doxorubicin-induced cardiomyopathy by inhibiting cell death via activating the Nrf2 pathway.Cardio-oncology (London, England) · 2024Article
- Red Ginseng Is a Therapeutic Candidate for Chronic Doxorubicin-Induced Cardiomyopathy in Mice.Evidence-based complementary and alternative medicine : eCAM · 2023Article
- Statins Show Anti-Atherosclerotic Effects by Improving Endothelial Cell Function in a Kawasaki Disease-like Vasculitis Mouse Model.International journal of molecular sciences · 2022Article
- CAWS administration increases the expression of interferon γ and complement factors that lead to severe vasculitis in DBA/2 mice.BMC immunology · 2013Article
- Etanercept suppresses arteritis in a murine model of kawasaki disease: a comparative study involving different biological agents.International journal of vascular medicine · 2013Article
- Anti-infective activity of simvastatin againstJournal of Indian Society of PeriodontologyArticle
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It was reported previously that a Candida albicans water-soluble fraction (CAWS), including a mannoprotein and β-glucan complex, has strong potency in inducing fatal necrotizing arteritis in DBA/2 mice. In this study, histopathological changes and cardiac function were investigated in this system. One mg/day of CAWS was given to DBA/2 mice via peritoneal injection for five days. The CAWS-treated DBA/2 mice were induced aortitis and died at an incidence of 100% within several weeks. Histological findings included stenosis in the left ventricular outflow tract (LVOT) and severe inflammatory changes of the aortic valve with fibrinoid necrosis. Cardiomegaly was observed and heart weight increased 1.62 fold (P < 0.01). Echocardiography revealed a severe reduction in contractility and dilatation of the cavity in the left ventricle (LV): LV fractional shortening (LVFS) decreased from 71% to 38% (P < 0.01), and the LV end-diastolic diameter (LVDd) increased from 2.21 mm to 3.26 mm (P < 0.01). The titer of BNP mRNA increased in the CAWS-treated group. Severe inflammatory changes resulting from CAWS brought about lethal LV dysfunction by aortic valve deformation with LVOT stenosis. This system is proposed as an easy and useful experimental model of heart failure because CAWS arteritis can be induced by CAWS injection alone.
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Registered trials
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