Background: Obesity is associated with chronic inflammation, which contributes to cardiovascular diseases. MicroRNAs (miRNAs) are reported to be involved in vascular inflammation and atherosclerosis. (AE) and metformin have been suggested to improve inflammation in vascular system. The aim of this study is to evaluate whether miRNAs are involved in high fat induced endothelial inflammation, and whether AE and metformin improve endothelial inflammation by regulating miRNAs.
Methods: We established high fat treated rats and human aortic endothelial cells (HAECs). AE and metformin were added to explore their effects on endothelial inflammation induced by high fat and the possible mechanism.
Results: The vascular inflammatory genes were increased in rats treated with high fat diet. The decreased miR-146a and miR-155 were involved in endothelial inflammation induced by high fat through targeting IL-1 receptor-associated kinase 1 (IRAK1), TNF receptor-associated factor 6 (TRAF6) and nuclear factor-κB p65 (NF-κB p65), respectively. While AE and metformin could ameliorate the endothelial inflammation by increasing miR-146a and miR-155.
Conclusions: These results indicate that miR-146a and miR-155 play roles in the high fat induced endothelial inflammation, which could be potential therapeutic targets. AE and metformin can attenuate endothelial inflammation through regulating miR-146a and miR-155.
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http://dx.doi.org/10.1186/s12986-020-00459-7 | DOI Listing |
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January 2025
Department of Operative Dentistry and Endodontics, Shanghai Stomatological Hospital and School of Stomatology, Fudan University, Shanghai, 200001, China.
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January 2025
Department of Pain, Fourth Affiliated Hospital of Harbin Medical University, Harbin, 150001, China.
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Indonesia Army Cellcure Center, Gatot Soebroto Central Army Hospital, Jakarta 10410, Indonesia.
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January 2025
Department of Medical Biotechnologies and Translational Medicine, University of Milan, 20125 Milan, Italy.
Venous thromboembolism (VTE) and arterial thrombosis (AT) are distinct yet closely related pathological processes. While traditionally considered separate entities, accumulating evidence suggests that they share common risk factors, such as inflammation and endothelial dysfunction (ED). This review explores the parallels and differences between venous and arterial thrombosis, with particular attention to the role of unprovoked VTE and its potential links to atherosclerosis and systemic inflammation.
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January 2025
Department of Rheumatology & Clinical Immunology, Amsterdam UMC, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands.
Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by inflammation leading to joint damage and systemic complications. Angiogenesis promotes inflammation and contributes to RA progression. This study evaluated potential anti-angiogenic effects of several compounds including small-molecule kinase inhibitors, such as sunitinib (pan-kinase inhibitor), tofacitinib (JAK-inhibitor), NIKi (NF-κB-inducing kinase inhibitor), and the integrin-targeting peptide fluciclatide, using a scratch assay and 3D spheroid-based models of angiogenesis.
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