ArticlePloS one2018
CD1d deficiency inhibits the development of abdominal aortic aneurysms in LDL receptor deficient mice.
Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- A review of current status of cell-based therapies for aortic aneurysms.Inflammation and regeneration · 2023Review
- Abdominal Aortic Aneurysm and PET/CT: From Molecular Mechanisms to Potential Molecular Imaging Targets.Reviews in cardiovascular medicine · 2023Review
- Activated invariant natural killer T cells infiltrate aortic tissue as key participants in abdominal aortic aneurysm pathology.Immunology · 2021Article
- A double-edged sword of immuno-microenvironment in cardiac homeostasis and injury repair.Signal transduction and targeted therapy · 2021Review
- Single-Cell Transcriptome Profiles Reveal Fibrocytes as Potential Targets of Cell Therapies for Abdominal Aortic Aneurysm.Frontiers in cardiovascular medicine · 2021Article
- Abdominal Aortic Aneurysm: Roles of Inflammatory Cells.Frontiers in immunology · 2020Review
- Abdominal aortic aneurysm: update on pathogenesis and medical treatments.Nature reviews. Cardiology · 2019Review
- Defective Autophagy in T Cells Impairs the Development of Diet-Induced Hepatic Steatosis and Atherosclerosis.Frontiers in immunology · 2018Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
An abdominal aortic aneurysm (AAA) is a dilatation of the abdominal aorta leading to serious complications and mostly to death. AAA development is associated with an accumulation of inflammatory cells in the aorta including NKT cells. An important factor in promoting the recruitment of these inflammatory cells into tissues and thereby contributing to the development of AAA is angiotensin II (Ang II). We demonstrate that a deficiency in CD1d dependent NKT cells under hyperlipidemic conditions (LDLr-/-CD1d-/- mice) results in a strong decline in the severity of angiotensin II induced aneurysm formation when compared with LDLr-/- mice. In addition, we show that Ang II amplifies the activation of NKT cells both in vivo and in vitro. We also provide evidence that type I NKT cells contribute to AAA development by inducing the expression of matrix degrading enzymes in vSMCs and macrophages, and by cytokine dependently decreasing vSMC viability. Altogether, these data prove that CD1d-dependent NKT cells contribute to AAA development in the Ang II-mediated aneurysm model by enhancing aortic degradation, establishing that therapeutic applications which target NKT cells can be a successful way to prevent AAA development.
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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.