lncRNA CDKN2B-AS1 is downregulated in patients with ventricular fibrillation in acute myocardial infarction.
Ricardo Pan-LizcanoLucía NúñezPablo PiñónGuillermo AldamaXacobe FloresRamón Calviño-SantosJosé Manuel Vázquez-RodríguezManuel Hermida-PrietoPublished in: PloS one (2024)
Ventricular fibrillation (VF) in acute myocardial infarction (AMI) is the main cause of deaths occurring in the acute phase of an ischemic event. Although it is known that genetics may play an important role in this pathology, the possible role of long non-coding RNAs (lncRNA) has never been studied. Therefore, the aim of this work is to study the expression of 10 lncRNAs in patients with and without VF in AMI. For this purpose, the expression of CDKN2B-AS1, KCNQ1OT1, LIPCAR, MALAT1, MIAT, NEAT1, SLC16A1-AS1, lnc-TK2-4:2, TNFRSF14-AS1, and UCA1 were analyzed. After the analysis and Bonferroni correction, the lncRNA CDKN2B-AS showed a statistical significance lower expression (P values of 2.514 x 10-5). In silico analysis revealed that six proteins could be related to the possible effect of lncRNA CDKN2B-AS1: AGO3, PLD4, POU4F1, ZNF26, ZNF326 and ZNF431. These in silico proteins predicted to have a low cardiac expression, although there is no literature indicating a potential relationship with VF in AMI. Thus, the lncRNA CDKN2B-AS1 shows a significant lower expression in patients with VF in AMI vs patients without VF in AMI. Literature data suggest that the role of CDKN2B1-AS is related to the miR-181a/SIRT1 pathway.
Keyphrases
- acute myocardial infarction
- long non coding rna
- poor prognosis
- left ventricular
- percutaneous coronary intervention
- long noncoding rna
- systematic review
- heart failure
- end stage renal disease
- oxidative stress
- ischemia reperfusion injury
- acute coronary syndrome
- molecular docking
- chronic kidney disease
- machine learning
- atrial fibrillation
- electronic health record
- big data
- data analysis