Intermittent High Glucose Exacerbates A-FABP Activation and Inflammatory Response through TLR4-JNK Signaling in THP-1 Cells.
Hui LiHan-Ying LuoQing LiuYang XiaoLin TangFeng ZhongGan HuangJun-Mei XuAi-Min XuZhi-Guang ZhouRu-Ping DaiPublished in: Journal of immunology research (2018)
Intermittent high glucose potentiates A-FABP activation and inflammatory responses via TLR4/p-JNK signaling in THP-1 cells. These findings suggest a more detrimental impact of glucose fluctuation on macrophage inflammation in diabetes-related vascular diseases than thus far generally assumed.
Keyphrases
- high glucose
- induced apoptosis
- inflammatory response
- endothelial cells
- oxidative stress
- cell cycle arrest
- endoplasmic reticulum stress
- signaling pathway
- cell death
- toll like receptor
- immune response
- cardiovascular disease
- type diabetes
- binding protein
- adipose tissue
- lps induced
- blood glucose
- nuclear factor
- pi k akt
- insulin resistance
- cell proliferation