<scp>miR</scp>‐92a aggravates metabolic syndrome via <scp>KLF2</scp>/<scp>miR</scp>‐483 axis
Endothelial dysfunction and fatty liver are critically involved in the pathogenesis of metabolic syndrome. MicroRNAs can mediate the cellular communication between vascular endothelial cells (ECs) and distal cell. Serum miR-92a level was higher in metabolic syndrome patients than controls. KLF2 is the target gene of miR-92a, which can increase the production of miR-483, miR-483 acts on its target genes CTGF, ET-1, and β-catenin to protect cell function. EC miR-92a is secreted out of cells into the blood, circulates through the blood to the liver, and continues to exert its biological effects after being absorbed by hepatocytes. LNA-miR-92a administration reversed endothelial cell damage and fatty liver caused by metabolic syndrome by affecting the KLF2/miR-483 pathway.
Authors
- Fenqing Shang (ORCID: https://orcid.org/0000-0002-8973-7118)
- Xia Yang (ORCID: https://orcid.org/0000-0002-8142-5857)
- Liang Bai (ORCID: https://orcid.org/0000-0002-4129-8662)
- Juan Pang (ORCID: https://orcid.org/0000-0001-6272-9890)
- Chaofeng Ma (ORCID: https://orcid.org/0000-0001-9834-8766)
- Hui Ding (ORCID: https://orcid.org/0000-0002-1602-9487)
- Longzhi Wang
- Haifeng Wang
- Feng Zhang (ORCID: https://orcid.org/0000-0002-0427-2842)
- Zhe Zhao (ORCID: https://orcid.org/0000-0003-0594-8928)
- W. Yang (ORCID: https://orcid.org/0000-0003-4909-8718)
- Jun Li (ORCID: https://orcid.org/0000-0001-8450-3702)
Institutions
- Northwest University (CN)
- Health First (US)
- Shaanxi Blood Center (CN)
- Xi'an Chest Hospital (CN)
- Xi'an Jiaotong University (CN)
Publication Details
- Journal
- Journal of Diabetes Investigation
- Published
- 2025-02-01
- DOI
- https://doi.org/10.1111/jdi.14416
- Citations
- 3
- Primary Topic
- Kruppel-like factors research
- Type
- article
- Field-Weighted Citation Impact
- 2.42
Funders
- National Natural Science Foundation of China