ArticleMediators of inflammation2014
Increased expression of chitinase 3-like 1 in aorta of patients with atherosclerosis and suppression of atherosclerosis in apolipoprotein E-knockout mice by chitinase 3-like 1 gene silencing.
Article in Mediators of inflammation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
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Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.
- Chitinase‑3 like‑protein‑1: A potential predictor of cardiovascular disease (Review).Molecular medicine reports · 2024Pooled it
- Uncovering molecular markers of the microvascular endothelial response in sepsis-associated acute kidney injury: a translational study in mice and humans.Intensive care medicine experimental · 2025Article
- Chitinase-3-like Protein 1 Reduces the Stability of Atherosclerotic Plaque via Impairing Macrophagic Efferocytosis.Journal of cardiovascular translational research · 2025Article
- Association between atherosclerosis and the development of multi-organ pathologies.SAGE open medicine · 2024Review
- Genetic Markers of Insulin Resistance and Atherosclerosis in Type 2 Diabetes Mellitus Patients with Coronary Artery Disease.Metabolites · 2023Review
- Article
- G721-0282 Exerts Anxiolytic-Like Effects on Chronic Unpredictable Mild Stress in Mice Through Inhibition of Chitinase-3-Like 1-Mediated Neuroinflammation.Frontiers in cellular neuroscience · 2022Article
- Chitinase 3 like 1 is a regulator of smooth muscle cell physiology and atherosclerotic lesion stability.Cardiovascular research · 2021Article
- Overexpression of chitotriosidase and YKL-40 in peripheral blood and sputum of healthy smokers and patients with chronic obstructive pulmonary disease.International journal of chronic obstructive pulmonary disease · 2019Article
- Atherosclerosis is exacerbated by chitinase-3-like-1 in amyloid precursor protein transgenic mice.Theranostics · 2018Article
- MicroRNA-mediated mechanisms of the cellular stress response in atherosclerosis.Nature reviews. Cardiology · 2015Review
- Site-Specific Secretome Map Evidences VSMC-Related Markers of Coronary Atherosclerosis Grade and Extent in the Hypercholesterolemic Swine.Disease markers · 2015Article
- Circulating YKL-40 level, but not CHI3L1 gene variants, is associated with atherosclerosis-related quantitative traits and the risk of peripheral artery disease.International journal of molecular sciences · 2014Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionThe purpose of this study was to investigate the changes of chitinase 3-like 1 (CHI3L1) in the aorta of patients with coronary atherosclerosis and to determine whether inhibition of CHI3L1 by lentivirus-mediated RNA interference could stabilize atherosclerotic plaques in apolipoprotein E-knockout (ApoE(-/-)) mice.
methodsWe collected discarded aortic specimens from patients undergoing coronary artery bypass graft surgery and renal arterial tissues from kidney donors. A lentivirus carrying small interfering RNA targeting the expression of CHI3L1 was constructed. Fifty ApoE(-/-) mice were divided into control group and CHI3L1 gene silenced group. A constrictive collar was placed around carotid artery to induce plaques formation. Then lentivirus was transfected into carotid plaques.
resultsWe found that CHI3L1 was overexpressed in aorta of patients with atherosclerosis and its expression was correlated with the atherosclerotic risk factors. After lentivirus transduction, mRNA and protein expression of CHI3L1 were attenuated in carotid plaques, leading to reduced plaque content of lipids and macrophages, and increased plaque content of collagen and smooth muscle cells. Moreover, CHI3L1 gene silencing downregulated the expression of local proinflammatory mediators.
conclusionsCHI3L1 is overexpressed in aorta from patients with atherosclerosis and the lentivirus-mediated CHI3L1 gene silencing could represent a new strategy to inhibit plaques progression.
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