ArticleThe Journal of biological chemistry2020
TL1A inhibits atherosclerosis in apoE-deficient mice by regulating the phenotype of vascular smooth muscle cells.
Article in The Journal of biological chemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
25 citing papers in PubMed, 36 citations in OpenAlex.
- ADAR1 and ADAR2 Expression in the Thoracic Aortic Wall Correlates with Aneurysm Severity and Dissection Risk: Insights into A-to-I RNA Editing Dysregulation in Marfan Syndrome-Derived vSMCs.International journal of molecular sciences · 2026Article
- VSMCs and the immune microenvironment: a multidimensional regulatory network driving vascular injury and repair.Frontiers in immunology · 2026Review
- Article
- IMM-H007 promotes hepatic cholesterol and triglyceride metabolism by activating AMPKActa pharmaceutica Sinica. B · 2025Article
- Arachidonic acid is involved in high-salt diet-induced coronary remodeling through stimulation of the IRE1α/XBP1s/RUNX2/OPN signaling cascade.Lipids in health and disease · 2025Article
- TNF superfamily molecules in atherosclerosis: mechanistic insights and therapeutic translation.Frontiers in immunology · 2025Review
- Hormonal influence: unraveling the impact of sex hormones on vascular smooth muscle cells.Biological research · 2024Review
- Deletion of Talin1 in Myeloid Cells Facilitates Atherosclerosis in Mice.Arteriosclerosis, thrombosis, and vascular biology · 2024Article
- The Intersection of HIV and Pulmonary Vascular Health: From HIV Evolution to Vascular Cell Types to Disease Mechanisms.Journal of vascular diseases · 2024Article
- High glucose promotes atherosclerosis by regulating miRNA let7d-5p level.Journal of diabetes investigation · 2024Article
- The Exacerbating Effects of the Tumor Necrosis Factor in Cardiovascular Stenosis: Intimal Hyperplasia.Cancers · 2024Review
- Model Systems to Study the Mechanism of Vascular Aging.International journal of molecular sciences · 2023Review
- Exploring cuproptosis as a mechanism and potential intervention target in cardiovascular diseases.Frontiers in pharmacology · 2023Review
- How vascular smooth muscle cell phenotype switching contributes to vascular disease.Cell communication and signaling : CCS · 2022Review
- Targeting the Crosstalk of Immune Response and Vascular Smooth Muscle Cells Phenotype Switch for Arteriovenous Fistula Maturation.International journal of molecular sciences · 2022Article
- Nanobiotechnology approaches for cardiovascular diseases: site-specific targeting of drugs and nanoparticles for atherothrombosis.Journal of nanobiotechnology · 2022Review
- The relationship between TNF-like protein 1A and coronary artery aneurysms in children with Kawasaki disease.Clinical and experimental medicine · 2022Article
- Role of advanced glycation end products on vascular smooth muscle cells under diabetic atherosclerosis.Frontiers in endocrinology · 2022Review
- Survey of Approaches for Investigation of Atherosclerosis In Vivo.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Survey of In Vitro Model Systems for Investigation of Key Cellular Processes Associated with Atherosclerosis.Methods in molecular biology (Clifton, N.J.) · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
TNF ligand-related molecule 1A (TL1A) is a vascular endothelial growth inhibitor to reduce neovascularization. Lack of apoE a expression results in hypercholesterolemia and atherosclerosis. In this study, we determined the precise effects of TL1A on the development of atherosclerosis and the underlying mechanisms in apoE-deficient mice. After 12 weeks of pro-atherogenic high-fat diet feeding and TL1A treatment, mouse aorta, serum, and liver samples were collected and used to assess atherosclerotic lesions, fatty liver, and expression of related molecules. We found that TL1A treatment significantly reduced lesions and enhanced plaque stability. Mechanistically, TL1A inhibited formation of foam cells derived from vascular smooth muscle cells (VSMCs) but not macrophages by activating expression of ABC transporter A1 (ABCA1), ABCG1, and cholesterol efflux in a liver X receptor-dependent manner. TL1A reduced the transformation of VSMCs from contractile phenotype into synthetic phenotypes by activating expression of contractile marker α smooth muscle actin and inhibiting expression of synthetic marker osteopontin, or osteoblast-like phenotype by reducing calcification. In addition, TL1A ameliorated high-fat diet-induced lipid metabolic disorders in the liver. Taken together, our work shows that TL1A can inhibit the development of atherosclerosis by regulating VSMC/foam cell formation and switch of VSMC phenotypes and suggests further investigation of its potential for atherosclerosis treatment.
Indexed as
Identifiers
What OpenQuestion holds
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.