ArticleJournal of diabetes investigation2022
Micro ribonucleic acid-363 regulates the phosphatidylinositol 3-kinase/threonine protein kinase axis by targeting NOTCH1 and forkhead box C2, leading to hepatic glucose and lipids metabolism disorder in type 2 diabetes mellitus.
Article in Journal of diabetes investigation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- USP18 mediates high glucose-induced cardiomyocyte injury by regulating the JAK/STAT signaling pathway through stabilizing FOXC2 expression.Journal of diabetes investigation · 2026Article
- Identification and verification of the key genes, CCR1 and EGR2, in diabetes-associated lipophagy.Scientific reports · 2026Article
- Transcriptomic responses and molecular mechanisms of glucagon-regulated glucose metabolism in Japanese flounder (Frontiers in physiology · 2026Article
- Impact of 4-Environment & health (Washington, D.C.) · 2025Article
- Comorbidity Genes of Alzheimer's Disease and Type 2 Diabetes Associated with Memory and Cognitive Function.International journal of molecular sciences · 2024Review
- Article
- Circulating microRNAs Showed Specific Responses according to Metabolic Syndrome Components and Sex of Adults from a Population-Based Study.Metabolites · 2022Article
- Micro ribonucleic acid-363 regulates the phosphatidylinositol 3-kinase/threonine protein kinase axis by targeting NOTCH1 and forkhead box C2, leading to hepatic glucose and lipids metabolism disorder in type 2 diabetes mellitus.Journal of diabetes investigation · 2022Article
- Qizhi Kebitong Formula Ameliorates Streptozocin-Induced Diabetic Osteoporosis through Regulating the PI3K/Akt/NF-BioMed research international · 2022Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
AIMS/
introductionGlucose metabolic disorder is the main cause for type 2 diabetes progression. Exploring the molecular mechanisms of metabolic disorder are crucial for type 2 diabetes treatment. MATERIALS AND
methodsMicro ribonucleic acid (miR)-363, NOTCH1 and forkhead box C2 (FOXC2) expressions in high glucose (HG)-treated HepG2 cells and the livers of type 2 diabetes mellitus rats were assessed using quantitative polymerase chain reaction. Protein levels of NOTCH1, FOXC2 and phosphatidylinositol 3-kinase (PI3K)/serine/threonine protein kinase (Akt)-related proteins were evaluated using western blot. Lipid accumulation was determined using Oil Red O staining. Then glucose consumption, blood glucose level and glycogen content were detected using kits. Finally, dual luciferase reporter assay was used to verify the binding relationship between miR-363 and NOTCH1, and the binding relationship between miR-363 and FOXC2.
resultsMiR-363 was significantly upregulated in the livers of diabetic rats and HG-induced HepG2 cells, whereas NOTCH1 and FOXC2 were downregulated. In HG-induced HepG2 cells, miR-363 inhibitor markedly increased glucose consumption and uptake, and reduced accumulation of lipid droplets. Then NOTCH1 and FOXC2 were identified as downstream targets of miR-363. NOTCH1 overexpression or FOXC2 overexpression could ameliorate glucose and lipids metabolism disorder in type 2 diabetes model cells. In addition, we found that FOXC2 inhibition abolished the effect of NOTCH1 overexpression on HG-induced HepG2 cells. Finally, we proved that the PI3K/Akt pathway was the downstream pathway of FOXC2.
conclusionMiR-363 was considered as a key regulator of glucose and lipids metabolism in type 2 diabetes mellitus, which regulated PI3K/Akt axis by targeting NOTCH1 and FOXC2, thus leading to hepatic glucose and lipids metabolism disorder in type 2 diabetes.
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