ArticlePloS one2014
Protective role for properdin in progression of experimental murine atherosclerosis.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
14 citing papers in PubMed, 24 citations in OpenAlex.
- Properdin deficiency or anti-properdin treatment ameliorates disease in the C3 gain-of-function mouse model of atypical haemolytic uraemic syndrome.Frontiers in immunology · 2026Article
- Endothelial Gsα deficiency promotes ferroptosis and exacerbates atherosclerosis in apolipoprotein E-deficient mice via the inhibition of NRF2 signaling.Acta pharmacologica Sinica · 2025Article
- Seventy Years Later: Systemic and Local Properdin in Atherosclerosis.Journal of the American Heart Association · 2025Article
- Alternative Complement Pathway in Carotid Atherosclerosis: Low Plasma Properdin Levels Associate With Long-Term Cardiovascular Mortality.Journal of the American Heart Association · 2025Article
- Canonical and non-canonical roles of complement in atherosclerosis.Nature reviews. Cardiology · 2024Review
- Contribution of animal models to the mechanistic understanding of Alternative Pathway and Amplification Loop (AP/AL)-driven Complement-mediated Diseases.Immunological reviews · 2023Review
- CFP is a prognostic biomarker and correlated with immune infiltrates in Gastric Cancer and Lung Cancer.Journal of Cancer · 2021Article
- Complement Properdin Regulates the Metabolo-Inflammatory Response to a High Fat Diet.Medicina (Kaunas, Lithuania) · 2020Article
- Clinical and functional consequences of anti-properdin autoantibodies in patients with lupus nephritis.Clinical and experimental immunology · 2020Article
- Properdin: A multifaceted molecule involved in inflammation and diseases.Molecular immunology · 2018Review
- The IL-1RI Co-Receptor TILRR (JACC. Basic to translational science · 2017Article
- Properdin: a tightly regulated critical inflammatory modulator.Immunological reviews · 2016Review
- The role of complement activation in atherogenesis: the first 40 years.Immunologic research · 2016Review
- Clinical and genetic factors associated with progression of geographic atrophy lesions in age-related macular degeneration.PloS one · 2015Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
Genetic, dietary and immune factors contribute to the pathogenesis of atherosclerosis in humans and mice. Complement activation is an integral part of the innate immune defence but also shapes cellular responses and influences directly triglyceride synthesis. Deficiency of Factor B of the alternative pathway (AP) of complement is beneficial in LDLR(-/-) mice fed a high fat diet. The serum glycoprotein properdin is a key positive regulator of the AP but has not been studied in experimental atherosclerosis. Atherosclerosis was assessed after feeding low fat (LFD) or high fat (HFD) Western type diets to newly generated LDLR(-/-) Properdin(KO) (LDLR(-/-)P(KO)) and LDLR-/-PWT mice. Lipids, lymphocytes and monocytes were similar among genotypes, genders and diets. Complement C3, but not C3adesarg, levels were enhanced in LDLR(-/-)P(KO) mice regardless of diet type or gender. Non-esterified fatty acids (NEFA) were decreased in male LDLR(-/-)P(KO) fed a HFD compared with controls. All mice showed significant atherosclerotic burden in aortae and at aortic roots but male LDLR(-/-) mice fed a LFD were affected to the greatest extent by the absence of properdin. The protective effect of properdin expression was overwhelmed in both genders of LDLR(-/-)mice when fed a HFD. We conclude that properdin plays an unexpectedly beneficial role in the development and progression of early atherosclerotic lesions.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.