ISSN 0371-0874, CN 31-1352/Q

Issue Archive

Identification of dysregulated microRNAs involved in arachidonic acid metabolism regulation in dilated cardiomyopathy-mediated heart failure patients

WANG Yan-Liang1,2, WANG Meng1,2, WANG Xiu-Jie1,2,*

1Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, China;2University of Chinese Academy of Sciences, Beijing 100049, China

Abstract

Heart failure (HF), a clinical syndrome with high morbidity and mortality, is becoming a growing public health problem. Dilated cardiomyopathy (DCM) is one of the major causes of HF, yet the molecular mechanisms underlying DCM-mediated HF are not completely understood. Previous studies have shown that dysregulation of arachidonic acid (AA) metabolism could contribute to the development of HF. To explore the roles of microRNAs (miRNAs) in regulating AA metabolism in HF, we used two public datasets to analyze the expression changes of miRNAs in the patients of DCM-mediated HF. A total of 101 and 88 miRNAs with significant abundance alterations in the two dataset were obtained, respectively. Around 1/3 of these miRNAs were predicted to target AA metabolic pathway genes. We also investigated the distribution of known single nucleotide polymorphisms (SNPs) within the sequences of miRNAs dysregulated in DCM-mediated HF patients, and identified miRNAs harboring high number of SNPs in either the seed regions or the entire sequences. These information could provide clues for further functional studies of miRNAs in the pathogeny of DCM-mediated HF. 


Key words: dilated cardiomyopathy; heart failure; microRNAs; arachidonic acid; single nucleotide polymorphisms

Received: 2021-03-12  Accepted: 2021-06-24

Corresponding author: 王秀杰  E-mail: xjwang@genetics.ac.cn

DOI: 10.13294/j.aps.2021.0062

Citing This Article:

WANG Yan-Liang, WANG Meng, WANG Xiu-Jie. Identification of dysregulated microRNAs involved in arachidonic acid metabolism regulation in dilated cardiomyopathy-mediated heart failure patients. Acta Physiol Sin 2021; 73 (4): 584-596