Our study indicates that Scd1, Cidea, Ghr, and Kl are downstream genes regulated by EZH2 in AKI. Upregulation of EZH2 in AKI inhibits the expression of these four genes in a different population of proximal tubular cells to minimize normal physiological function and promote acute or chronic cell injuries following AKI.
Keyphrases
- acute kidney injury
- poor prognosis
- long non coding rna
- ischemia reperfusion injury
- single cell
- long noncoding rna
- induced apoptosis
- genome wide
- liver failure
- genome wide identification
- bioinformatics analysis
- cell cycle arrest
- oxidative stress
- drug induced
- cell proliferation
- signaling pathway
- respiratory failure
- cell therapy
- type diabetes
- cell death
- genome wide analysis
- metabolic syndrome
- extracorporeal membrane oxygenation
- dna methylation
- transcription factor
- adipose tissue
- intensive care unit
- acute respiratory distress syndrome
- growth hormone