Overexpression Of hsa-miR-664a-3p Is Associated With Cigarette Smoke-Induced Chronic Obstructive Pulmonary Disease Via Targeting FHL1.
Shan ZhongChengshui ChenNaijia LiuLi YangZhangli HuPengfei DuanDiquan ShuaiQing-Ying ZhangYun WangPublished in: International journal of chronic obstructive pulmonary disease (2019)
The present study validated significant upregulation of hsa-miR-664a-3p in COPD patients, and its target gene FHL1 was downregulated and positively correlated with FEV1/FVC%; both hsa-miR-664a-3p and FHL1 could be regulated by cigarette smoke extract. Results of bioinformatic analyses and expanded validation suggest that the axis from hsa-miR-664a-3p to FHL1 might play a key role in cigarette smoke-induced COPD, and the exact mechanism should be confirmed in further studies.
Keyphrases
- chronic obstructive pulmonary disease
- lung function
- high glucose
- end stage renal disease
- diabetic rats
- cell proliferation
- newly diagnosed
- oxidative stress
- ejection fraction
- drug induced
- chronic kidney disease
- prognostic factors
- peritoneal dialysis
- signaling pathway
- poor prognosis
- transcription factor
- genome wide
- copy number
- endothelial cells
- cystic fibrosis
- air pollution
- long non coding rna
- patient reported outcomes
- dna methylation
- drug delivery
- genome wide identification