ArticleMolecular medicine (Cambridge, Mass.)2022
miR-351 promotes atherosclerosis in diabetes by inhibiting the ITGB3/PIK3R1/Akt pathway and induces endothelial cell injury and lipid accumulation.
Article in Molecular medicine (Cambridge, Mass.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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18 citing papers in PubMed, 29 citations in OpenAlex.
- Macrophage PIM1 Drives Atherosclerosis by Enhancing Foam Cell Formation Via CD36.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- AIBP deficiency drives MAFLD advancement via ITGβ3 mediated lipid metabolism disruption and pro-inflammatory activation.Cell communication and signaling : CCS · 2026Article
- Compound Danshen decoction identifies its mechanism of antagonizing atherosclerosis by network pharmacology and transcriptomics.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Integrin β3 Orchestrates Hepatic Steatosis via a Novel CD36-Dependent Lipid Uptake Complex.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Transcriptomics-based identification of shared biomarkers across type 2 diabetes, mild cognitive impairment, and uric acid metabolism.Experimental biology and medicine (Maywood, N.J.) · 2026Article
- Study on the Mechanism of Bifidobacterium animalis subsp. lactis F1-3-2 Regulating Bile Acid Metabolism Through TMA-TMAO Pathway to Improve Atherosclerosis.Probiotics and antimicrobial proteins · 2025Article
- Macrophage PIM1 Drives Atherosclerosis by Enhancing Foam Cell Formation Via CD36.bioRxiv : the preprint server for biology · 2025Article
- PSIP1 promotes gefitinib resistance in lung adenocarcinoma by inducing the expression of WASF3 and its downstream ITGB3/AKT signaling.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025Article
- Differential effects of Mediterranean vs. Western diets on coronary atherosclerosis and peripheral artery transcriptomics.Frontiers in nutrition · 2025Article
- Enhanced glycolysis induced by activation of AKT/NF-κB signaling pathway contributes to doxorubicin resistance in DLBCL.American journal of cancer research · 2025Article
- Crosstalk between MiRNAs/lncRNAs and PI3K/AKT signaling pathway in diabetes mellitus: Mechanistic and therapeutic perspectives.Non-coding RNA research · 2024Review
- Bioinformatics Analysis and Experimental Findings Reveal the Therapeutic Actions and Targets ofJournal of diabetes research · 2024Article
- ITCH-Mediated Ubiquitylation of ITGB3 Promotes Cell Proliferation and Invasion of Ectopic Endometrial Stromal Cells in Ovarian Endometriosis.Biomedicines · 2023Article
- The role of oxidative stress in diabetes mellitus-induced vascular endothelial dysfunction.Cardiovascular diabetology · 2023Review
- Review
- Noncoding RNAs as Key Regulators for Cardiac Development and Cardiovascular Diseases.Journal of cardiovascular development and disease · 2023Review
- Oxidative Stress Modulation by ncRNAs and Their Emerging Role as Therapeutic Targets in Atherosclerosis and Non-Alcoholic Fatty Liver Disease.Antioxidants (Basel, Switzerland) · 2023Review
- Angiogenesis induction using organoid-tissue modules: A platform for modular vessel construction.Journal of tissue engineeringArticle
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe miR-351 gene is significantly upregulated in diabetic mice with atherosclerosis. However, the mechanism by which its presence is important for the overall disease has not been elucidated. Therefore, this study will investigate the mechanism of miR-351 in the process of diabetes mellitus with atherosclerosis through miR-351 gene knockout mice.
methodsIn this study, miR-351
resultsThe expression of the miR-351 gene was significantly increased in the high-fat wild-type (HWT) group, and its expression was significantly decreased in the knockout mice. Silencing miR-351 effectively alleviated atherosclerosis in mice. The levels of miR-351 expression, apoptosis, lipid accumulation, and oxidative stress in ox-LDL + high glucose-induced endothelial cells were significantly increased. These phenomena were effectively inhibited in lentivirus-infected miR-351-silenced cell lines. Bioinformatics predicted that miR-351-5p could directly target the ITGB3 gene. Transfection of ITGB3 siRNA reversed the downregulation of apoptosis, decreased oil accumulation, and decreased oxidative stress levels induced by miR-351 silencing. In addition, it inhibited the activation of the PIK3R1/Akt pathway.
conclusionSilencing miR-351 upregulates ITGB3 and activates the PIK3R1/Akt pathway, thereby exerting anti-apoptosis and protective effects on endothelial cells.
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