A20 prevents obesity-induced development of cardiac dysfunction.
Wenjing XuCheng WangMinglu LiangLong ChenQin FuFengxiao ZhangYan WangDan HuangCheng WangPublished in: Journal of molecular medicine (Berlin, Germany) (2017)
A20 expression is downregulated in obesity-related hearts. A20 ameliorates HFD-induced lipid accumulation, ROS, inflammation, apoptosis, hypertrophy, fibrosis, and cardiac dysfunction. A20 represses TAK1 activation and the downstream inhibition of P38, JNK1/2, and the NF-κB pathway. TAK1 overexpression retards the beneficial effects of A20.
Keyphrases
- oxidative stress
- diabetic rats
- high glucose
- cell death
- insulin resistance
- metabolic syndrome
- type diabetes
- weight loss
- signaling pathway
- dna damage
- induced apoptosis
- weight gain
- drug induced
- poor prognosis
- high fat diet induced
- high fat diet
- cell proliferation
- mouse model
- endothelial cells
- endoplasmic reticulum stress
- transcription factor
- binding protein
- lps induced
- heart failure
- nuclear factor