ArticleDiabetes2012
Silence of TRIB3 suppresses atherosclerosis and stabilizes plaques in diabetic ApoE-/-/LDL receptor-/- mice.
Article in Diabetes, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 49 citations in OpenAlex.
- TRIB3 Links Endoplasmic Reticulum Stress to Impaired Efferocytosis in Atherosclerosis.Circulation research · 2025Article
- TRIB3 mediates vascular calcification by facilitating self-ubiquitination and dissociation of Smurf1 in chronic kidney disease.The Journal of clinical investigation · 2025Article
- Computational-experimental strategy identifies Co-upregulated biomarkers linking coronary heart disease and type 2 diabetes pathogenesis.Frontiers in genetics · 2025Article
- Therapeutic mechanism of Pithecellobium clypearia Benth. on imiquimod-induced psoriasis revealed by tissue transcriptomics in mice.PloS one · 2025Article
- Lack of alpha CGRP exacerbates the development of atherosclerosis in ApoE-knockout mice.Scientific reports · 2024Article
- Article
- Integration of dietary nutrition and TRIB3 action into diabetes mellitus.Nutrition reviews · 2024Review
- Brown adipose tissue-derived Nrg4 alleviates endothelial inflammation and atherosclerosis in male mice.Nature metabolism · 2022Article
- CHOP Increases TRIB3-Dependent miR-208 Expression to Potentiate Vascular Smooth Muscle Cell Proliferation and Migration by Downregulating TIMP3 in Atherosclerosis.Cardiovascular drugs and therapy · 2022Article
- Tribbles 3 deficiency promotes atherosclerotic fibrous cap thickening and macrophage-mediated extracellular matrix remodelling.Frontiers in cardiovascular medicine · 2022Article
- Endoplasmic reticulum stress and unfolded protein response in cardiovascular diseases.Nature reviews. Cardiology · 2021Review
- Extracorporeal shock wave therapy combined with engineered mesenchymal stem cells expressing stromal cell-derived factor-1 can improve erectile dysfunction in streptozotocin-induced diabetic rats.Translational andrology and urology · 2021Article
- Control of Cell Growth and Proliferation by the Tribbles Pseudokinase: Lessons from Drosophila.Cancers · 2021Review
- Modulation of TRIB3 and Macrophage Phenotype to Attenuate Insulin Resistance After Downhill Running in Mice.Frontiers in physiology · 2021Article
- PTPN2 improved renal injury and fibrosis by suppressing STAT-induced inflammation in early diabetic nephropathy.Journal of cellular and molecular medicine · 2019Article
- Whole-Genome Linkage Scan Combined With Exome Sequencing Identifies Novel Candidate Genes for Carotid Intima-Media Thickness.Frontiers in genetics · 2018Article
- Efficient Promotion of Autophagy and Angiogenesis Using Mesenchymal Stem Cell Therapy Enhanced by the Low-Energy Shock Waves in the Treatment of Erectile Dysfunction.Stem cells international · 2018Article
- ADisease models & mechanisms · 2017Article
- Cellular and Molecular Mechanisms of Diabetic Atherosclerosis: Herbal Medicines as a Potential Therapeutic Approach.Oxidative medicine and cellular longevity · 2017Review
- Assessment of Human Tribbles Homolog 3 Genetic Variation (rs2295490) Effects on Type 2 Diabetes Patients with Glucose Control and Blood Pressure Lowering Treatment.EBioMedicine · 2016Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Insulin resistance triggers the developments of diabetes mellitus and atherosclerosis. Tribbles homolog 3 (TRIB3) is involved in insulin resistance. We aimed to investigate whether TRIB3 is implicated in diabetic atherosclerosis. Sixty 3-week-old apolipoprotein E (ApoE-/-)/LDR receptor (LDLR-/-) mice were randomly divided into chow and diabetes groups. Diabetes was induced by a high-fat and high-sugar diet combined with low-dose streptozotocin. Mice in both groups were randomly divided into vehicle and TRIB3-silencing groups. After transfection, all mice were killed to evaluate the effects of TRIB3 on atherosclerosis. Silence of TRIB3 markedly decreased insulin resistance (P=0.039) and glucose (P=0.019), regardless of diabetes. Ultrasonography-measured parameters were similar in both groups, with and without silence of TRIB3. However, silence of TRIB3 decreased the aortic atherosclerotic burden (P=1×10(-13)). Further study showed that in brachiocephalic lesions, fibrous cap thickness, cap-to-core ratio, collagen content, and the number of smooth muscle cells were significantly increased (P<0.01 for all) by silence of TRIB3, whereas lipid and macrophage contents remained unaltered, with the vulnerability index significantly reduced. Moreover, the numbers of apoptotic cells and macrophages in brachiocephalic lesions were both significantly decreased (P<0.01 for both). Macrophage migration was decreased (P=4×10(-4)) by knocking down TRIB3, whereas adhesion and phagocytosis were increased (P<0.05 for both). Silence of TRIB3 would diminish atherosclerotic burden and increase the plaque stability in diabetic mice.
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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.